Differential diagnosis of common tremor syndromes

Tremor is one of the most common involuntary movement disorders seen in clinical practice. It is defined as an involuntary, approximately rhythmic, and roughly sinusoidal movement of one or more body parts. It is differentiated from other involuntary movement disorders, such as chorea, athetosis, ballism, tics, and myoclonus, by its repetitive, stereotyped movements of a regular amplitude and frequency. Tremor may be confused with rhythmic myoclonus (incorrectly termed cortical tremor), which is typically characterised by brief muscle twitches, confined to one limb or to adjacent body regions, associated with spike-wave complexes on the electroencephalogram (EEG) or spinal lesions. Clonus, unlike tremor, represents a rhythmic movement, which is increased by muscle stretching. Asterixis can be distinguished from tremor on the basis of electromyographic (EMG) findings of prolonged absence of EMG activity during “flapping” or abduction of the upper extremities. Stereotypies may have rhythmic components, but nevertheless are dominanted by complex movements. Lastly, epilepsia partialis continua (EPC) can produce regular jerks of the arm or hand, which can be difficult to distinguish from tremor. EPC is associated with EEG changes (which may need to be identified with back-averaging techniques), and MRI changes in contralateral sensorimotor cortex.

The first step in evaluating any patient with tremor is to characterise the tremor. Various types of tremor can be distinguished clinically, based on the activation condition, frequency, and topographical distribution. Different classifications of tremor have been proposed although the most useful and widely accepted classification divides tremor according to the behaviour it occurs, that is rest and action tremor, which is further subdivided into postural and kinetic tremor (table 1).^1–3 Action tremor, the most prevalent of these types of tremor, occurs during sustained extension of the arm and during voluntary movements, such as writing or typing. Resting tremor is suspected, if it occurs with the patient sitting with his arms firmly supported without any voluntary activities, if it increases with mental stress (counting backwards), and if it is suppressed by voluntary movements. The most common cause of resting tremor is idiopathic Parkinson’s disease (PD). The most common cause of postural and kinetic tremor is essential tremor (ET). Physiological tremor is an action tremor and is present in every healthy person under certain conditions. Tremor can present alone or as part of a neurological syndrome, for example multiple sclerosis, dystonia, and neuropathy. This article discusses different types of tremor with an emphasis on salient features and how to distinguish them clinically. Evidence supporting various available strategies is then presented, followed by a review of established guidelines.

Table 1

 Classification of tremor

ESSENTIAL TREMOR: THE MOST COMMON FORM OF ACTION TREMOR

Action tremor refers to any tremor that is produced by voluntary contraction of muscles, including postural, isometric, and kinetic tremor. The last includes intention tremor. As there are no validated serological, radiological, and pathological markers in ET, the diagnosis is primarily based on clinical findings (box 1).² Therefore, the examination should be comprehensive. Firstly, observe the patient sitting at rest to note whether there is evidence of a resting tremor of the head, hands, or legs. Then, ask the patient to stretch out the arms and hands completely and look for a postural tremor, followed by checking finger-nose-finger movements looking for a kinetic tremor. Typically, essential tremor is an action tremor, either postural or kinetic in character, mainly affecting the hands. It is usually bilateral with a frequency of 4 Hz to 12 Hz and largely symmetrical.⁴ The upper limbs are affected in about 95% of patients, followed by head (34%), lower limbs (20%), voice (12%), face and trunk (5%).² With the passage of time, the frequency of the tremor decreases and the amplitude may increase. ⁵ The prevalence ranges from 0.4% to 6.7% in persons over 40 years old so it is the most common type of tremor.^6–8 Many studies have shown that ET is much more prevalent than tremor of PD (up to 20 times difference).^9,10 However, some experts suspected that the condition might be overdiagnosed.¹¹ Although the condition is both clinically and genetically heterogeneous, half of the cases are considered familial with an autosomal dominant pattern of inheritance.^9,12–14 Two different chromosomal regions have been linked to familial ET, one on chromosome 3q13¹⁵ and another on chromosome 2p22–25.¹⁶ However, no specific gene mutations have been identified to date. The penetrance is thought to be high, suggesting that 89% of patients at risk have signs of ET by the age of 65.^6,17 The age of onset is typically 60–70 years, but not uncommonly before 60 years, and both sexes are equally affected. The tremor commonly involves the head, jaw, neck, facial muscles, tongue, and upper extremities but not the lip, which suggests the tremor of PD in those cases.

Box 1

Clinical criteria for essential tremor²

Definite essential tremor

• Postural tremor of moderate amplitude is present in at least one arm

• Tremor of moderate amplitude is present in at least one arm during at least four tasks, such as pouring water, using a spoon to drink water drinking water, finger-to-nose manoeuvre, and drawing a spiral.

• Tremor must interfere with at least one activity of daily living.

• Medications, hypothyroidism, alcohol, and other neurological conditions are not the cause of tremor.

Probable essential tremor

• Tremor of moderate amplitude is present in at least one arm during at least four tasks, or head tremor is present.

• Medications, hyperthyroidism, alcohol, and other neurological conditions are not the cause of tremor.

Clinically, the differentiation between ET and tremor of PD can be difficult (table 2). However, important features that support the tremor to be parkinsonian in origin include asymmetric onset and it being at rest although 40% of tremor in PD can be of mixed type of postural and resting tremors. Tremor that occurs during walking usually suggests an underlying diagnosis of PD. In addition, patients with ET typically lack prominent extrapyramidal signs, including bradykinesia, manifesting as progressive decrement in amplitude and speed with “re-setting”, postural instability or rigidity. Fifty per cent of ET patients are alcohol responsive but only temporarily.¹⁸ Sometimes, it can be difficult to determine if bradykinesia is present in a patient with pronounced postural tremor. In these circumstances, other factors such as the presence of hypomimia and generalised bradykinesia may need to be taken into account. A “no-no” or “yes-yes” head tremor is characteristic of ET and occurs only rarely in PD. Handwriting is usually small and illegible in PD but large and tremulous in ET (fig 1). If a noticeable tremor is noted with speaking, ET is probable in most cases with a possibility of isolated voice tremor in a minority. Most patients with ET do not have abnormal neurological findings except the tremor although signs of mild cerebellar dysfunction can be seen, supported by a recent study using positron emission tomography (PET) showing increased cerebellar activation.¹⁹ When the presentation is atypical, functional brain imaging with positron emission tomography and the radiotracer 18-fluorodopa (FDOPA-PET) may permit the diagnosis of PD in early stage, recording and quantifying the deficiency of dopamine synthesis and storage within pre-synaptic striatal nerve terminals. In addition, dopamine transporter (DAT) single photon emission computed tomography (SPECT), such as ¹²³I-ß-FP-CIT, can effectively distinguish between ET and PD in an early stage of the disease with the results being within normal limits in ET.^20,21 Apart from excluding the possibility of early PD, a careful drug history is mandatory as many drugs are capable of producing postural and kinetic tremors (box 2). These drugs include β-adrenergic agonists, valproic acid, thyroxin, tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), and lithium. These drugs may cause increased physiological tremor that may be difficult to distinguish it from ET. Therefore, clinicians must maintain a high level of suspicion when a tremor develops after the start of a drug treatment. The possibility of Wilson’s disease should always be considered in any patient with an action tremor who is younger than 40 years of age. A low serum ceruloplasmin is useful screening test although not diagnostic and the level of less than 200 mg/l has 95% sensitivity for this condition. A slit-lamp examination for Kayser-Fleischer ring should also be considered. However, patients with Wilson’s disease usually present with dysarthria, dystonia, and parkinsonism and very rarely present with isolated action tremor.²²

Table 2

 Features differentiating tremor of PD from ET⁷²

Figure 1

 Comparison of handwriting in patients with PD (top) and ET (bottom). Note that the handwriting in PD is small and illegible in contrast with ET, which is large and tremulous.

Box 2

Commonly used drugs that may cause tremor

ET is believed to be of a central nervous system origin, but a reproducible neuropathology has not been described. A central aetiology was partly supported by the beneficial effect of thalamotomy, thalamic deep brain stimulation (DBS), and drugs that act centrally. Numerous experimental physiological and functional imaging studies have also implicated dysfunction in brain stem structures, including the inferior olive, locus coeruleus, red nucleus, thalamus, but cerebellum seems to be a prime candidate for the site of dysfunction in ET.^23–25 It is probable that ET occur as a result of an abnormal oscillator of a CNS “pacemaker” in a currently unknown exact location that can be increased or suppressed by reflex pathways.

Unfortunately, pharmacological treatment of ET remains unsatisfactory. Probably, ET is not as benign as it is often referred as benign essential or familial tremor. About 15%–25% of patients with ET retire prematurely and 60% of patients choose not to apply for a job or promotion because of the uncontrollable shaking of their hands.⁴ The two most often used drugs are non-selective β blockers (for example, propranolol) and primidone. Because these drugs can result in multiple side effects, especially during the titration phase, they are not recommended for mild cases that do not cause dysfunction or social embarrassment. Tremor of different body parts and various tremor subtypes may also have different pharmacological responsiveness. In general, the start of specific pharmacological treatments is typically based on patient age, coexistent conditions, prior exposure to drug therapy, concurrent drug therapies, contraindications, physician and patient bias, as well as benefits and potential adverse effects of certain agents. Drug dose is initially low, gradually titrated upward as tolerated, and adjusted as appropriate to identify the most efficacious dose with a minimum of adverse effects (regulation of dose). If the drug is of no benefit at a dose that causes adverse effects, dose levels are gradually tapered down and treatment is eventually stopped. If a drug is reported to be beneficial, it may be continued at the regulated doses and the next drug may be added to the drug regimen. If the response to a drug is adequate and the dose well tolerated, the physician may keep the patient at the same dose or decide to increase the dose level (and continue to monitor tolerance). Propranolol, a non-selective antagonist, is more effective than selective β₁ activity, with the dose of at least 120 mg/day resulting in a significant reduction in the severity of tremor.^26,27 In a dose response study of propranolol, 240–320 mg/day was found to be the optimal dose range.²⁸ Furthermore, long acting propranolol (propranolol LA) has been shown to be equally effective as conventional propranolol and has better compliance.²⁹ Propranolol is generally well tolerated. However, relative contraindications, including asthma, heart failure, arterioventricular block, and diabetes mellitus, have limited its use in some patients. The mechanism of propranolol in ET is not exactly known although central and peripheral mechanisms have been proposed.^30,31 In general, 50%–70% of patients obtain symptomatic relief from propranolol, but dramatic improvement occurs in a much smaller percentage. Similarly, primidone, an anticonvulsant in doses of up to 750 mg/day, has been shown to be effective than placebo in reducing tremor. Although initial tolerability has limited the use of primidone, we find that slow titration, beginning as low as 12.5 mg/day, may lessen side effects (mainly drowsiness) and increase tolerability. The mechanism of action of primidone’s antitremor effect is also unknown. Phenobarbital is one of primidone’s active metabolites but it has little, if any, antitremor effect on its own. Common reported side effects include nausea, vertigo, drowsiness, and unsteadiness. Koller et al³² showed in a placebo controlled study that primidone (50–1000 mg/day) significantly reduced the amplitude of hand tremor in both untreated and propranolol treated patients. There was no correlation between therapeutic response and serum concentrations. Neither drug was conclusively shown to be superior to the other but more patients had a preference for primidone than for propranolol in one study.³³

In addition to the first line treatments, many other drugs have been used as monotherapy or adjunctive treatment. Topiramate has been shown to be effective as well as gabapentin and alprazolam.^34,35 Theophylline, flunarizine, olanzapine have been used with variable success. Intramuscular injections of botulinum toxin type A into intrinsic hand muscles can be considered in medically resistant cases.³⁶ Lastly, DBS in the ventral intermedius nucleus (VIM) of the thalamus in ET (Activa Tremor Control Therapy) is effective, with over 90% of patients having a satisfactory result. Because this rate of improvement cannot generally be achieved with current pharmacological therapy and several long term studies have also shown the long term efficacy, the Food and Drug Administration (FDA) has approved this device for medically intractable cases and it has now replaced thalamotomy.^37,38

PARKINSONIAN TREMOR: THE MOST COMMON FORM OF RESTING TREMOR

The tremor in PD typically occurs at rest and becomes less prominent with voluntary movement. It typically occurs initially in the distal upper extremity, and over time, moves proximally and then to the other upper extremity, again in a distal to proximal pattern. Seventy per cent of patients with PD present with tremor and it usually has a better prognosis, compared with PD patients with early postural instability and akinesia. Action or postural tremor does occur in PD, either alone or in combination, making the diagnosis difficult in some cases, especially in the early stage.¹ In fact, pure rest tremor is infrequent in PD; more common is the combination of rest and postural kinetic tremors. Isolated postural and kinetic tremor rarely occurs in PD. As a result of the variability of the clinical expression of tremors in PD, the definition is based on the general diagnosis of PD rather than on specific features of tremors. Only the rest tremor component is by itself, a positive diagnostic criterion for PD but other tremors are often seen. When the diagnosis is unclear, levodopa trial may be considered to record the remarkable improvement in patients with PD. In contrast with akinesia and rigidity, the response of parkinsonian tremor to dopaminergic treatment can be so variable and it is the overall improvement that counts and supports the diagnosis.³⁹ A variety of agents have been used for tremor in PD, including levodopa, dopamine agonists, anticholinergics, budipine, and as second line treatments, clozapine, propranolol, and clonazepam.⁴⁰ However, double blind, randomised trials specifically assessing their efficacy in tremor in early PD are few with different methodologies and the results are variable.^40–42 Anticholinergics, such as trihexylphenidyl, have been shown to be effective but rarely used now because of its side effects, especially in the elderly population.⁴³ Therefore, anticholinergics are not generally recommended to patients with cognitive decline or elderly patients over 65 years of age. Both dopaminergic and anticholinergics are probably equally effective in parkinsonian tremor, but dopaminergic substances additionally improve other parkinsonian signs. Dopamine agonists, such as pramipexole and ropinirole, are probably the most effective antitremor drugs among all dopaminergic treatments and should be considered in all newly diagnosed tremor predominant PD patients who have no cognitive impairment.^44–46 Improvement of tremor has also been reported with other dopamine agonists, including pergolide and bromocriptine.^47,48 Dopamine agonists are also useful in advanced PD patients with tremor that is refractory to levodopa and anticholinergics.⁴⁵ As for akinesia and rigidity, after longer disease duration the additional use of levodopa may become necessary for adequate control of resting tremor in many patients.

Some patients have a predominant postural tremor in addition to their rest tremor. This form is uncommon and has been considered to be a combination of an ET with PD although the relation between postural tremor that is phenomenologically similar to ET and PD has not been well defined. Further studies are needed to define the relation between ET and other tremors, including PD and other task specific tremors.

WHAT IS THE PHYSIOLOGICAL TREMOR?

Physiological tremor is seen in all normal people when muscles are activated. The tremor is typically postural and is thought to arise from the resonant oscillation of a limb as a result of mechanical factors affecting it. Because the physiological tremor has 8–12 Hz, and α rhythm in the electroencephalogram has a similar frequency (7–13 Hz), a common central hypothesis was raised.⁴⁹ Physiological tremor can be barely visible to the naked eye and does not interfere with activities of daily living. The frequency of physiological tremor is <6 Hz before age 9 years, increasing to 12 Hz by the mid-teen years, and decreasing slightly above 60 years. The frequency usually decreases when large inertia loads are applied to the limb, as shown with accelerometry and electromyography.⁵⁰ The amplitude is typically so low as to be virtually undetectable under normal circumstances. Increased physiological tremor is defined by the easy visibility of high frequency, postural tremor with no evidence of an underlying neurological disease.¹ Furthermore, the cause is usually reversible. Certain conditions can exacerbate physiologic tremor, for example stress and anxiety before public performance. Indeed, some professional performers have learned to avoid this response by taking a β blocker before the event. Fatigue because of lack of sleep and consuming a large amount of caffeine can be precipitating factors although one study did not find physiological tremor to be significantly increased by caffeine.⁵¹ Relaxation sessions have been shown to decrease tremor significantly.⁵² In general, no drugs are usually warranted. However, a small dose of propranolol can be useful in some people, for example ophthalmic surgeons, when fine coordinative movements are required.⁴⁰ Other conditions that can augment physiological tremor include thyrotoxicosis, pheochromocytoma, hypoglycaemia, withdrawal from opioids or sedatives.

Tremor is a common side effect of many drugs (box 2 lists commonly used drugs that can cause tremor). Various drugs and toxins can cause all types of tremor known clinically although increased physiological tremor is most commonly seen. Tremor is the dose limiting side effect of the β₂ adrenergic agonists, salbutamol and terbutaline, used to treat obstructive airway diseases. Tremor is usually seen within a month of starting valproic acid treatment and is more evident when a dose is >750 mg/day although it can also occur when the dose is within therapeutic range. It is the most common tremorogenic drug among anticonvulsants, affecting up to 25% of patients.⁵³ Intention tremor may occur in patients on lithium. The occurrence rate increases with increasing serum lithium levels and manifests almost 100% in patients with lithium toxicity.⁵⁴ Tardive tremor, a rare disorder, represents a separate entity in which, by definition, is caused by exposure to a dopamine receptor blocking agent (DRBA) within six months of the onset of symptoms and persisting for at least one month after stopping the offending drug. ⁵⁵ It is usually static in nature but can occur at rest and on intentional movements, such as eating and writing. Tremor can also occur as a toxic reaction to marijuana, and 3,4-methylene-dioxymethamphetamine or ecstasy.⁵⁶

CEREBELLAR TREMOR

Classic cerebellar tremor is often termed as intention tremor. The tremor is typically of low frequency below 5 Hz. It is characteristically kinetic in nature and has an added volitional component and particularly affects the head and the upper half of the body. Postural tremor may be present, but rest tremor is usually absent. When kinetic tremor occurs or worsens as the target is reached, it is referred to as terminal tremor. In rare occasions, cerebellar tremor also has a rest component in which case it would be described as Holmes’ tremor. In cerebellar tremor, the oscillations are of variable amplitude and are perpendicular to the direction of movement. It is usually best elicited during the finger-nose-finger or heel-shin-heel tests. Furthermore, cerebellar tremor is often associated with dysmetria, dyssynergia, and hypotonia. Titubation is another tremor that is probably a result of abonormality of the cerebellum or its afferent/efferent pathways and is a slow frequency oscillation depending on postural innervation. Its rhythmicity is, at times, the only sign distinguishing it from ataxia of the trunk. Multiple sclerosis is a common cause of cerebellar tremor. Other causes include Friedreich’s ataxia, spinocerebellar degeneration, and cerebellar infarction. Although no clear correlations between cerebellar lesions and tremor have been established, lesions in the superior cerebellar peduncle and dentate nucleus are the most common reported sites resulting in intention tremor.^57,58

Unfortunately, there is no established pharmacological treatment for cerebellar tremor. The results of medical treatment are often less than satisfactory. However, as multiple neurotransmitters as well as feedback pathways, including brain stem, thalamus and cortical neurons, seem to be involved, several drugs have been tried, but with variable success, including odansetron (5-HT₃ antagonist), isoniazid, physostigmine, carbamazepine, and clonazepam. ^59,60 In refractory cases, chronic DBS of the VIM (or less commonly nucleus ventralis oralis posterior and zona incerta) may provide an alternative.^61,62 Although few studies used highly standardised quantitative outcome measures, and follow up periods were generally one year or less, the data suggested that chronic DBS of the VIM produced improved tremor control in multiple sclerosis.⁶¹ However, complete cessation of tremor is generally not achieved. There were some reported cases in which tremor control decreased over time, and frequent reprogramming became necessary.

PSYCHOGENIC TREMOR

The criteria suggestive of psychogenic tremor are sudden onset but rarely a remitting course (box 3). The onset is mostly associated with a stressful life event. According to a modified Fahn’s criteria for psychogenic dystonia, the diagnosis of psychogenic tremor is accepted with the followings; (1) the major causes of symptomatic tremors (such as medications, thyroid dysfunction, and hormonal or metabolic dysfunction) have been excluded, (2) essential and parkinsonian tremors are excluded on the basis of clinical criteria, (3) no evidence for any other neurological disorders is present, and (4) the patients had a period without tremor of at least two weeks during the observation period. ⁶³ The tremor of psychogenic in origin is usually a combination of resting and postural or intention tremors and most often involves both arms, followed by the head and then the legs. The tremor may be continuous or intermittent with fluctuating frequency and amplitude, but lacks the physiological pattern. As mentioned, the onset is usually abrupt (73%) with maximal disability (46%) at the onset that had static course in 46% and fluctuating course in 17%.⁶⁴ Although certain criteria are provided for the diagnosis of psychogenic tremor, the diagnosis can be obvious in patients with generalised shaking.^63,65 In these instances, the shaking usually stops during the examination as they are exhausting for patients. Differential diagnosis in this setting is limited, but includes orthostatic tremor, essential stance tremors, or the rare stance tremor of PD.

Box 3

Clinical features suggestive of psychogenic tremor⁷³

• Abrupt onset

• Static course

• Spontaneous remission

• Unclassified tremor (complex tremors)

• Clinical inconsistencies

• Changing tremor characteristics

• Unresponsive to antitremor drugs

• Tremor increases with attention, and lessens with distractibility

• Responsive to placebo

• Absence of other neurological signs

• Multiple somatisations

• Multiple underdiagnosed conditions

• Spontaneous remissions or cures of symptoms

• No evidence of disease by laboratory or radiological investigations

• Employed in allied health professionals

• Litigation or compensation pending

• Presence of secondary gain

• Presence of psychiatric disease

• Reported functional disturbances in the past

The examination, especially the two clinical signs, are very useful in this situation; the entrainment of tremor frequency and the coactivation sign. ⁶⁶ Entrainment entails requiring the patient to maintain a tapping rhythm in an uninvolved body part (finger or foot) at a different frequency than the suspicious tremor. A psychogenic tremor automatically changes to the frequency that is being enforced on the uninvolved hand or foot, because it is difficult to maintain two different volitional movement frequencies simultaneously in two different body parts. During passive movement of the involved limb, an increased tone can be palpated by the examiner. Once the increased tone disappears, the tremor also disappears (coactivation sign). Cogwheeling in the setting of PD and ET differs from the present coactivation sign as the first is present over the whole range of movement of a particular joint. In contrast, coactivation in psychogenic tremor resembles voluntary coactivation with overlying rhythmic trembling. In addition, coactivation can produce bizarre positioning of the hands when they are outstretched. The absence of finger tremor is also suggestive of psychogenic in origin. While physiological and pathological tremors show a decrease of tremor amplitude when postural with and without loading is compared, psychogenic tremor tends to show an increase of their tremor amplitudes during loading.

Commonly, patients with psychogenic tremor often undergo a large number of diagnosis and therapeutic procedures before the final diagnosis is established. A review of medical history in these patients usually shows multiple functional somatic or psychosomatic illnesses. Once the diagnosis is made, most patients continue to have a fluctuating or constant course, followed by improving and progressive periods suggesting the prognosis is far from benign. The therapeutic success is also variable, but the treatment approach should include various combinations of psychotherapy as well as drugs, such as mild anxiolytics and antidepressants. While pharmacological treatment in organic tremor may reduce amplitude, but does not change the tremor frequency, the effect of treatment in psychogenic tremor usually varies from total suppression of tremor, especially when associated with the suggestion of a “cure” to no benefit.²⁶ Interestingly, most of successfully treated patients were young.⁶³

OTHER TYPES OF TREMOR

In addition to the tremors described above, they are other forms of tremor that are less common and some of them have only been reported in a few case studies. Of these, dystonic tremor is worth mentioning as many patients with dystonia have tremor and it is sometimes difficult to distinguish dystonic tremors from static tremors associated with dystonia, which occur unspecifically in regions unaffected by dystonia. Dystonic tremor is mainly a postural and kinetic tremor in an extremity or body part affected by dystonia and is not usually seen during complete rest.¹ It is now considered as a distinct entity from ET, as it is irregular, has a broad range of frequencies (mainly less than 7 Hz), and remains localised. A typical example is tremulous spasmodic torticollis. The tremor tends to be localised, asymmetric, and irregular in amplitude and periodicity. Many patients with dystonic tremor use their own tricks (geste antagoniste or sensory tricks) to reduce the tremor amplitude. These together with the absence of attempts at suppressing the tremor by voluntary muscle contractions are a fairly reliable diagnostic sign. Head tremor is common in patients with cervical dystonia and treatment with botulinum toxin often results in significant improvement of tremor as well as dystonia.

Orthostatic tremor is a rare disorder of middle aged or elderly people that is characterised by unsteadiness on standing, secondary to 16 Hz tremor in the lower extremities. Characteristically, the tremors remit on walking, but disappear when sitting or lying down.¹ Patients prefer to stand on a wide base but walk normally and only a fine ripple of muscle activity is visible. Confirmation of the diagnosis can be obtained by EMG showing a 16 Hz pattern in the leg muscles with the patient standing. In terms of treatment, the drug most commonly used is clonazepam, followed by levodopa and then drugs used for ET. Overall, the treatment response seems to be unsatisfactory, but some success has been reported with gabapentin (300–2400 mg/day) in a small placebo controlled, double blind, crossover trial.⁶⁷

Holmes’ tremor is a term, proposed by the Ad Hoc Scientific Committee on Movement Disorders, to refer to previously used midbrain tremor, rubral tremor, thalamic tremor, myorhythmia, and Benedikt’s syndrome.¹ It is a symptomatic tremor of predominantly proximal limbs of low frequency (<4.5 Hz) during postural in nature, worsening during movement and goal directed tasks. Like cerebellar tremor, Holmes’ tremor is almost always attributable to lesions, reported in upper brain stem, thalamus, or cerebellum, interrupting pathways in the midbrain tegmentum (rubro-olivocerebellorubral loop, rubrospinal fibres, nigrostriatal fibres), and the serotonergic brain stem telencephalic fibres.⁶⁸ Palatal tremor, previously termed palatal myoclonus, can be either symptomatic attributable to brain stem and/or cerebellar lesions or essential without any identified brain lesions. In symptomatic palatal tremor, inferior olivary pseudohypertrophy is seen and considered as a hallmark for the condition.^69,70 Sleep does not abolish the symptoms. In essential cases, patients usually have characteristic ear clicks (rhythmic movements of the tensor veli palatini muscle), which do not present in a symptomatic variety. Botulinum toxin injection into each tensor veli palatini has been reported to be of some benefits.⁷¹ Tremors, mostly postural and kinetic, can also develop in patients with some forms of peripheral neuropathy, particularly demyelinating neuropathies (especially dysgammaglobulinaemic neuropathies). The term “cortical tremor” is a misnomer as it is not a tremor but a specific form of rhythmic myoclonus.⁶⁸ Distinguishing rhythmic myoclonus from tremor (particularly Holmes’ tremor) can be difficult because the driving muscle contractions can be so brisk resulting in longer pauses between individual jerks.

Tremor is a common problem seen in clinical practice. Among all types of tremor, essential tremor is the most common cause. In most cases of tremor, there is no diagnostic laboratory test to confirm or exclude a particular type of tremor and the diagnosis heavily relies on physician’s own observation and thorough clinical examination as well as clinical history. In persons younger than 40 years of age, the possibility of Wilson’s disease should be excluded, as it is a treatable and reversible condition if recognised promptly. Differentiation between essential tremor and tremor of PD is particularly important as the management and prognosis in these two conditions are vastly different. Almost all drugs used to treat tremor should be titrated slowly as side effects and tolerability are the main issues of compliance. The treatment should be evidence based. We recommend that the first line treatments, if available, should be firstly attempted, followed by second line treatments that are supported by prospective clinical trials before finally choosing drugs from anecdotal evidence.

REFERENCES

1. ↵

   Deuschl G, Bain P, Brin M. Consensus statement of the Movement Disorder Society on Tremor. Ad Hoc Scientific Committee. Mov Disord1998;13 (suppl 3) :2–23.

2. ↵

   Elble RJ. Diagnostic criteria for essential tremor and differential diagnosis. Neurology2000;54:S2–6.

3. ↵

   Grimes DA. Tremor—easily seen but difficult to describe and treat. Can J Neurol Sci2003;30 (suppl 1) :S59–63.

4. ↵

   Louis, ed. Clinical practice. Essential tremor. N Engl J Med2001;345:887–91.

5. ↵

   Elble RJ. Essential tremor frequency decreases with time. Neurology2000;55:1547–51.

6. ↵

   Brin MF, Koller W. Epidemiology and genetics of essential tremor. Mov Disord1998;13 (suppl 3) :55–63.

7. Bharucha NE, Bharucha EP, Bharucha AE, et al. Prevalence of Parkinson’s disease in the Parsi community of Bombay, India. Arch Neurol1988;45:1321–3.

8. ↵

   Haerer AF, Anderson DW, Schoenberg BS. Prevalence of essential tremor. Results from the Copiah County study. Arch Neurol1982;39:750–1.

9. ↵

   Louis ED, Ford B, Frucht S, et al. Risk of tremor and impairment from tremor in relatives of patients with essential tremor: a community-based family study. Ann Neurol2001;49:761–9.

10. ↵

    Bain PG, Findley LJ, Thompson PD, et al. A study of hereditary essential tremor. Brain1994;117:805–24.

11. ↵

    Schrag A, Munchau A, Bhatia KP, et al. Essential tremor: an overdiagnosed condition? J Neurol2000;247:955–9.

12. ↵

    Louis ED, Ford B, Barnes LF. Clinical subtypes of essential tremor. Arch Neurol2000;57:1194–8.

13. Louis ED, Barnes LF, Ford B, et al. Ethnic differences in essential tremor. Arch Neurol2000;57:723–7.

14. ↵

    Jankovic J. Essential tremor: a heterogenous disorder. Mov Disord2002;17:638–44.

15. ↵

    Gulcher JR, Jonsson P, Kong A, et al. Mapping of a familial essential tremor gene, FET1, to chromosome 3q13. Nat Genet1997;17:84–7.

16. ↵

    Higgins JJ, Pho LT, Nee LE. A gene (ETM) for essential tremor maps to chromosome 2p22–p25. Mov Disord1997;12:859–64.

17. ↵

    Rautakorpi I, Takala J, Marttila RJ, et al. Essential tremor in a Finnish population. Acta Neurol Scand1982;66:58–67.

18. ↵

    Chouinard S, Louis ED, Fahn S. Agreement among movement disorder specialists on the clinical diagnosis of essential tremor. Mov Disord1997;12:973–6.

19. ↵

    Wills AJ, Jenkins IH, Thompson PD, et al. A positron emission tomography study of cerebral activation associated with essential and writing tremor. Arch Neurol1995;52:299–305.

20. ↵

    Asenbaum S, Pirker W, Angelberger P, et al. [123I]beta-CIT and SPECT in essential tremor and Parkinson’s disease. J Neural Transm1998;105:1213–28.

21. ↵

    Benamer TS, Patterson J, Grosset DG, et al. Accurate differentiation of parkinsonism and essential tremor using visual assessment of [123I]-FP-CIT SPECT imaging: the [123I]-FP-CIT study group. Mov Disord2000;15:503–10.

22. ↵

    Roberts EA, Schilsky ML. A practice guideline on Wilson disease. Hepatology2003;37:1475–92.

23. ↵

    Deuschl G, Elble RJ. The pathophysiology of essential tremor. Neurology2000;54:S14–20.

24. Deuschl G, Wenzelburger R, Loffler K, et al. Essential tremor and cerebellar dysfunction clinical and kinematic analysis of intention tremor. Brain2000;123:1568–80.

25. ↵

    Wilms H, Sievers J, Deuschl G. Animal models of tremor. Mov Disord1999;14:557–71.

26. ↵

    Larsen TA, Calne DB. Essential tremor. Clin Neuropharmacol1983;6:185–206.

27. ↵

    Dietrichson P, Espen E. Effects of timolol and atenolol on benign essential tremor: placebo-controlled studies based on quantitative tremor recording. J Neurol Neurosurg Psychiatry1981;44:677–83.

28. ↵

    Koller WC. Dose-response relationship of propranolol in the treatment of essential tremor. Arch Neurol1986;43:42–3.

29. ↵

    Cleeves L, Findley LJ. Propranolol and propranolol-LA in essential tremor: a double blind comparative study. J Neurol Neurosurg Psychiatry1988;51:379–84.

30. ↵

    Young RR. Essential-familial tremor and other action tremors. Semin Neurol1982;2:386–91.

31. ↵

    Jefferson D, Jenner P, Marsden CD. beta-Adrenoreceptor antagonists in essential tremor. J Neurol Neurosurg Psychiatry1979;42:904–9.

32. ↵

    Koller WC, Royse VL. Efficacy of primidone in essential tremor. Neurology1986;36:121–4.

33. ↵

    Gorman WP, Cooper R, Pocock P, et al. A comparison of primidone, propranolol, and placebo in essential tremor, using quantitative analysis. J Neurol Neurosurg Psychiatry1986;49:64–8.

34. ↵

    Connor GS. A double-blind placebo-controlled trial of topiramate treatment for essential tremor. Neurology2002;59:132–4.

35. ↵

    Ondo W, Hunter C, Vuong KD, et al. Gabapentin for essential tremor: a multiple-dose, double-blind, placebo-controlled trial. Mov Disord2000;15:678–82.

36. ↵

    Brin MF, Lyons KE, Doucette J, et al. A randomized, double masked, controlled trial of botulinum toxin type A in essential hand tremor. Neurology2001;56:1523–8.

37. ↵

    Koller W, Pahwa R, Busenbark K, et al. High-frequency unilateral thalamic stimulation in the treatment of essential and parkinsonian tremor. Ann Neurol1997;42:292–9.

38. ↵

    Limousin P, Speelman JD, Gielen F, et al. Multicentre European study of thalamic stimulation in parkinsonian and essential tremor. J Neurol Neurosurg Psychiatry1999;66:289–96.

39. ↵

    Koller WC, Hubble JP. Levodopa therapy in Parkinson’s disease. Neurology1990;40 (suppl) :40–7.

40. ↵

    Wasielewski PG, Burns JM, Koller WC. Pharmacologic treatment of tremor. Mov Disord1998;13 (suppl 3) :90–100.

41. Koller WC. Pharmacologic treatment of parkinsonian tremor. Arch Neurol1986;43:126–7.

42. ↵

    Hughes AJ, Lees AJ, Stern GM. Apomorphine in the diagnosis and treatment of parkinsonian tremor. Clin Neuropharmacol1990;13:312–17.

43. ↵

    Katzenschlager R, Sampaio C, Costa J, et al. Anticholinergics for symptomatic management of Parkinson’s disease. Cochrane Library. Issue 2. Oxford: Update Software, 2003.

44. ↵

    Navan P, Findley LJ, Jeffs JA, et al. Double-blind, single-dose, cross-over study of the effects of pramipexole, pergolide, and placebo on rest tremor and UPDRS part III in Parkinson’s disease. Mov Disord2003;18:176–80.

45. ↵

    Pogarell O, Gasser T, van Hilten JJ, et al. Pramipexole in patients with Parkinson’s disease and marked drug resistant tremor: a randomised, double blind, placebo controlled multicentre study. J Neurol Neurosurg Psychiatry2002;72:713–20.

46. ↵

    Schrag A, Keens J, Warner J. Ropinirole for the treatment of tremor in early Parkinson’s disease. Eur J Neurol2002;9:253–7.

47. ↵

    Korczyn AD, Brunt ER, Larsen JP, et al. A 3-year randomized trial of ropinirole and bromocriptine in early Parkinson’s disease. The 053 Study Group. Neurology1999;53:364–70.

48. ↵

    van Laar T, Lledo A, Quail D, et al. An analysis of the improvement in activities of daily living (ADL) and motor score associated with pergolide monotherapy in the treatment of Parkinson’s disease. Eur J Neurol1999;6:133.

49. ↵

    Pizzuti GP, Byford GH, Cifaldi S, et al. Finger tremor and the central nervous system. J Biomed Eng1992;14:356–9.

50. ↵

    Deuschl G, Raethjen J, Lindemann M, et al. The pathophysiology of tremor. Muscle Nerve2001;24:716–35.

51. ↵

    Koller W, Cone S, Herbster G. Caffeine and tremor. Neurology1987;37:169–72.

52. ↵

    Comby B, Chevalier G, Bouchoucha M. A new method for the measurement of tremor at rest. Arch Int Physiol Biochim Biophys1992;100:73–8.

53. ↵

    Karas BJ, Wilder BJ, Hammond EJ, et al. Valproate tremors. Neurology1982;32:428–32.

54. ↵

    Vestergaard P. Clinically important side effects of long-term lithium treatment: a review. Acta Psychiatr Scand Suppl1983;305:1–36.

55. ↵

    Stacy M, Jankovic J. Tardive tremor. Mov Disord1992;7:53–7.

56. ↵

    Demirkiran M, Jankovic J, Dean JM. Ecstasy intoxication: an overlap between serotonin syndrome and neuroleptic malignant syndrome. Clin Neuropharmacol1996;19:157–64.

57. ↵

    Finsterer J, Muellbacher W, Mamoli B. Yes/yes head tremor without appendicular tremor after bilateral cerebellar infarction. J Neurol Sci1996;139:242–5.

58. ↵

    Thach WT, Goodkin HP, Keating JG. The cerebellum and the adaptive coordination of movement. Annu Rev Neurosci1992;15:403–42.

59. ↵

    Sandyk R. Successful treatment of cerebellar tremor with clonazepam. Clin Pharm1985;4:615–18.

60. ↵

    Trelles L, Trelles JO, Castro C, et al. Successful treatment of two cases of intention tremor with clonazepam. Ann Neurol1984;16:621.

61. ↵

    Wishart HA, Roberts DW, Roth RM, et al. Chronic deep brain stimulation for the treatment of tremor in multiple sclerosis: review and case reports. J Neurol Neurosurg Psychiatry2003;74:1392–7.

62. ↵

    Nandi D, Aziz TZ. Deep brain stimulation in the management of neuropathic pain and multiple sclerosis tremor. J Clin Neurophysiol2004;21:31–9.

63. ↵

    Deuschl G, Koster B, Lucking CH, et al. Diagnostic and pathophysiological aspects of psychogenic tremors. Mov Disord1998;13:294–302.

64. ↵

    Kim YJ, Pakiam AS, Lang AE. Historical and clinical features of psychogenic tremor: a review of 70 cases. Can J Neurol Sci1999;26:190–5.

65. ↵

    Koller W, Lang A, Vetere-Overfield B, et al. Psychogenic tremors. Neurology1989;39:1094–9.

66. ↵

    Uddin MK, Rodnitzky RL. Tremor in children. Semin Pediatr Neurol2003;10:26–34.

67. ↵

    Onofrj M, Thomas A, Paci C, et al. Gabapentin in orthostatic tremor: results of a double-blind crossover with placebo in four patients. Neurology1998;51:880–2.

68. ↵

    Samie MR, Selhorst JB, Koller WC. Post-traumatic midbrain tremors. Neurology1990;40:62–6.

69. ↵

    Deuschl G, Toro C, Valls-Sole J, et al. Symptomatic and essential palatal tremor. 1. Clinical, physiological and MRI analysis. Brain1994;117:775–88.

70. ↵

    Deuschl G, Toro C, Hallett M. Symptomatic and essential palatal tremor. 2. Differences of palatal movements. Mov Disord1994;9:676–8.

71. ↵

    Cho JW, Chu K, Jeon BS. Case of essential palatal tremor: atypical features and remarkable benefit from botulinum toxin injection. Mov Disord2001;16:779–82.

72. ↵

    Bhidayasiri R, Waters MF, Giza CC. Neurological differential diagnosis: a prioritized approach. Oxford: Blackwell, 2005.

73. ↵

    Manyam BV. Uncommon forms of tremor. In: Watts RL, Koller WC, eds. Movement disorders:neurologic principles and practice. 2nd ed. New York: McGraw-Hill, 2004:459–80.

Causes of Tremor Other than Parkinson’s

A tremor doesn’t always mean it’s Parkinson’s

Many people think of Parkinson’s disease (PD) as the “tremor disease”, so much so, that when a tremor is noticed, the first diagnosis people typically think of is PD. Although about 25% of people with PD do not have tremor, 75% of them do, so tremor is certainly a very visible and characteristic symptom of PD.

However, there are many other medical conditions that can cause a tremor. Today, we will discuss the features of various tremors, other medical conditions that can manifest with tremor, and the clues that distinguish a PD tremor from other types of tremor.

Rest vs. postural vs. action tremor

A tremor is defined as movement of a body part that oscillates rhythmically around a midpoint.

When deciding whether a tremor is consistent with a diagnosis of PD, the most important feature is the position of the body part in which the tremor occurs. There are three main positions to consider.

Rest tremor

A rest tremor occurs when a body part is not being held against gravity and is not moving. Rest tremors occur for example, when the hands are resting in the lap, such as when watching television, or when the arms are dangling at the side when walking.

Postural tremor

A postural tremor occurs when a body part is held against gravity. Postural tremors occur for example, when the arms are extended, such as when holding a tray.

Kinetic tremor

A kinetic tremor occurs when a body part is moving. Kinetic tremors occur for example, when the arm is moving toward the mouth to eat.

Parkinson’s tremors classically occur at two characteristic times. One is at rest. The other is when the limb is moved and then held against gravity. The tremor tends to stop during the movement and then resume in the new posture. This is referred to as a re-emergent tremor.

Although there are many diseases that cause tremor in general, there are very few that cause rest tremor and re-emergent tremor. So if a person can accurately distinguish between these entities, this can be an important clue in diagnosing PD. However, to the untrained eye, it can be very difficult to distinguish between these tremors. Therefore, if you have a tremor, it is best to get checked out by a neurologist.

Identifying a tremor

Frequency of tremor

A PD tremor typically has a frequency of about 3-6 Hz, which means that the body part moves back and forth about 3-6 times a second. This can be variable however, with younger people tending to have faster tremors. Therefore, the frequency of the tremor is not characteristic enough to use as a means of diagnosing a PD tremor.

Affected body part

A PD tremor most commonly affects the fingers or hand, but can also affect the legs and jaw. Almost universally, the tremor of PD is asymmetric, meaning that it is different on each side of the body. Typically, the tremor starts on one side and even if, as the disease progresses, it begins to affect the other side, a difference between the two sides of the body tends to remain.

PD tremors do not commonly affect the head or neck (which results in the head moving in a “yes-yes” or “no-no” direction) or vocal cords (which results in a shaky voice when holding a note).

The term “pill rolling” is often used in reference to a PD tremor. This refers to a repetitive circular motion of the thumb against the other fingers. Although this is a pattern that is sometimes seen, there are many other characteristic rest tremors of PD, such as bending and unbending at the wrist or rotation at the wrist.

The company it keeps

Perhaps most important of all in deciding whether a tremor is consistent with PD or another disorder is determining whether other symptoms of PD are present, in addition to the tremor. The symptoms that can occur early in in the disease and provide evidence that the tremor is part of PD include:

• decreased blink rate
• small handwriting, that decreases in size as the writing continues
• small, movements of the hands and the feet, worse on one side
• characteristic stiffness of the arms and the legs, worse on one side
• stooped posture
• decreased arm swing on one side while walking
• the characteristic walk in which the whole foot is planted flat at one time – instead of the heel being planted on the ground first
• the characteristic way of turning by taking multiple steps and not pivoting

Other causes of tremor besides Parkinson’s disease

There are numerous other medical conditions that can cause postural or kinetic tremor, and these are considered during evaluation of a tremor:

Exaggerated physiologic tremor

Every person has an innate tremor that is typically very subtle, but will emerge when hungry, angry, nervous or otherwise activated. A common example of this is a tremor that becomes prominent when speaking in public. This tremor is typically fast, ranging from 5-10 Hz. Some people’s innate tremor is more prominent than others and they may notice it and be worried about it. This type of tremor however, is not of concern.

Essential tremor

Essential tremor (ET) is very common, affecting about 4 percent of the population in those aged 65 and older. (This is about 4 times more common than PD). ET is characterized by a kinetic tremor which usually involves the arms, but can involve the legs, head or voice.

People with essential tremor have particular difficulties with tasks that require making accurate movements. This includes bringing food to the mouth with a utensil – particularly soup which can easily slosh off the spoon. People with ET find that using two hands to do tasks makes things easier, so they will typically use two hands to bring a mug to the mouth or to use a screwdriver.

The tremor can range in severity, from mild to extremely severe. The tremor can occur at any age and cases in children have been reported. However, the prevalence markedly increases with age.  In about 50% of people, there is a clear family history of tremor. Despite the fact that so many people with ET have a family history of the condition, the search for genes that cause ET has been slow.

In many cases of ET, the tremor is alcohol responsive. This means that the tremor is improved with alcohol. Because it can be a characteristic feature, a neurologist will often ask about alcohol responsiveness when he/she is evaluating a tremor.

A mild rest tremor can be seen in someone with long-standing ET. In addition, instability with walking can also be seen in someone with long-standing ET.

Treatments include use of medications such as beta-blockers and primidone. Deep brain stimulation (DBS) is a surgical treatment in which thin electrodes introduce electric impulses in specific parts of the brain. DBS of the thalamus is very effective for ET and is used for severe cases. (DBS is also a treatment for PD, with the electrodes inserted in a different location in the brain) Focused ultrasound, a technology in which beams of ultrasound waves are focused on a particular part of the brain, thereby concentrating enough energy to create a small lesion, is the newest FDA-approved treatment for ET.

Drug-induced tremor

A wide variety of medications can cause tremor. Drug-induced tremors typically are symmetric or equal on both sides of the body. The medications that can cause tremor include, but are not limited to, lithium, valproic acid, amiodarone, beta-adrenergic agonists, and selective serotonin reuptake inhibitors (SSRIs). Be attentive to whether a tremor starts after any new medication is started. If it does, discuss this with your doctor.

It is important to distinguish between medications that cause tremor (listed above) and medications that cause PD-like symptoms, including PD-like tremors.  Medications that cause PD-like symptoms are ones that block dopamine and should be avoided in people with PD. Here is a table of medications to be avoided in PD.

Metabolic disorders

Certain metabolic disturbances such as hyperthyroidism (or excessive production of thyroid hormone) can lead to a tremor. Typically, this condition can be distinguished from a pure tremor disorder by symptoms that accompany the tremor. These can include weight loss, palpitations, excessive sweating, nervousness, and a tendency to be overheated.  However, in a person with a new tremor, checking levels of thyroid hormone makes sense. Hypoglycemia or low glucose can similarly cause tremor. The tremor of hypoglycemia is also typically accompanied by other symptoms including sweating, dizziness, hunger and irritability.

Dystonic tremor

Dystonic tremor occurs as part of dystonia, a movement disorder in which repetitive and sustained muscle contractions result in twisting movements of a body part. A common body part that is subject to a dystonic tremor is the neck. Dystonia of the neck results in repetitive twisting of the neck in a particular direction. These repetitive movements of the neck may take on the qualities of a tremor, resulting in a dystonic tremor.  It is sometimes hard to distinguish between essential tremor of the neck and dystonic tremor of the neck. A movement disorders physician often needs to be consulted to make this distinction.

Neuropathic tremor

Tremor can be a sign of a neuropathy, a disorder of the peripheral nerves, or the nerves that bring messages from the brain and spinal cord to rest of the body. In particular, neuropathies caused by autoimmune syndromes such as chronic inflammatory demyelinating polyneuropathy (CIDP) can have tremor as a component. Tremor in this situation is not an isolated symptom but is evaluated in the context of other symptoms of CIDP which can include weakness, numbness and tingling. An evaluation by a neurologist can determine if neuropathic tremor is a diagnostic consideration.

Orthostatic tremor

Orthostatic tremor is a relatively uncommon tremor of the legs which occurs primarily when a person is standing but not when sitting or walking. The tremor is very rapid (12-18 Hz) and a person typically complains of shaking legs and a fear of falling when standing still. The shaking causes the affected person to constantly try to sit or walk instead of stand.

Rubral tremor

A rubral tremor is a relatively slow tremor which is present both at rest and action. It is caused by a lesion in specific areas deep in the brain. The lesion could be a bleed, a stroke, or a tumor.  The tremor usually emerges during recovery from a major neurologic event and does not present simply as a tremor.

Cerebellar tremor

A cerebellar tremor manifests as a specific type of kinetic tremor known as an intention tremor, one that worsens when trying to accurately reach a target. There may be minimal tremor on the way to the target, but it increases substantially when approaching and trying to accurately hit the target. A cerebellar tremor is caused by a problem in the cerebellum, the part of the brain that controls accuracy of movement. There are a whole host of causes of cerebellar problems including specific genetic diseases, as well as brain lesions such as bleeds, strokes or tumors.

Other neurodegenerative diseases

Atypical parkinsonian syndromes such as Multiple System Atrophy (MSA) can have tremor as one of its symptoms.

There are other, more uncommon neurodegenerative diseases apart from PD and atypical parkinsonian syndromes that can manifest with tremor. Two of these include Wilson’s disease and Fragile X Tremor Ataxia Syndrome (FXTAS). These diseases have complex symptomatology and the larger neurologic picture aids in making the diagnosis.

Tips and takeaways

• There are many causes of tremor besides PD so you should not automatically think anyone with a tremor must have PD.
• Not everyone with PD has a tremor (25% do not).
• When a tremor arises, it should be evaluated by a neurologist who can test for particular features of the tremor as well as look for other neurologic symptoms to help make a diagnosis.
• PD tremors typically occur at rest and are accompanied by subtle signs of other motor problems, which can help to distinguish it from other causes of tremor.
• Always bring any new symptom, such as a tremor, to the attention of your medical team.

Do you have a question or issue that you would like Dr. Gilbert to explore? Suggest a Topic

Dr. Rebecca Gilbert

APDA Vice President and Chief Scientific Officer

Dr. Gilbert received her MD degree at Weill Medical College of Cornell University in New York and her PhD in Cell Biology and Genetics at the Weill Graduate School of Medical Sciences. She then pursued Neurology Residency training as well as Movement Disorders Fellowship training at Columbia Presbyterian Medical Center. Prior to coming to APDA, she was an Associate Professor of Neurology at NYU Langone Medical Center. In this role, she saw movement disorder patients, initiated and directed the NYU Movement Disorders Fellowship, participated in clinical trials and other research initiatives for PD and lectured widely on the disease.

View all posts by Dr. Rebecca Gilbert

A Closer Look ArticlePosted in Living with Parkinson’s, Parkinson’s Disease Symptoms

DISCLAIMER: Any medical information disseminated via this blog is solely for the purpose of providing information to the audience, and is not intended as medical advice. Our healthcare professionals cannot recommend treatment or make diagnoses, but can respond to general questions. We encourage you to direct any specific questions to your personal healthcare providers.

Frequently Asked Questions: Essential Tremor

How can you tell the difference between essential tremor and Parkinson’s disease?

Essential tremor is a neurological disorder that causes tremors, generally of both hands, but also the head and voice. It is often confused with Parkinson’s disease, but the tremor in essential tremor is an action tremor, which means that the tremor is most noticeable when the limb is in use or moving (e.g. writing, eating, drinking a glass of water) and improves when the limb is at rest. This is opposite of the tremor seen in Parkinson’s disease, which is most noticeable when the limbs are relaxed and at rest, and lessens when the affected limb is in use.

Who is affected by essential tremor?

Up to 10 million Americans are estimated to have essential tremor; 10 times the number of people with Parkinson’s disease. ET affects males and females equally across a multiracial population. Individuals with a clear family history of tremor are at greater likelihood of developing ET. However, it can occur in individuals without a clear family history. While it can start at any age, onset is most common in middle age.

Can my children get essential tremor?

Children of individuals with ET have a greater likelihood of having the condition, although some may never experience symptoms. A variant in the gene LINGO1 has been identified as a risk gene, although not all individuals with ET carry this variant—which can also be present in people without ET. For those affected, the areas impacted and severity of symptoms can vary from person to person. 

Does essential tremor get worse over time?

Typically, ET symptoms gradually worsen over time. While most people with ET only experience mild to moderate symptoms as they age, others may experience substantial disability. As it progresses, tremor frequency (number of repetitions per second) may decrease; however, tremor amplitude (magnitude/strength) may increase, which can cause challenges with fine, discrete motor skills such as writing or eating. With treatment, symptoms can be managed.

What medications are typically prescribed to treat essential tremor?

There are several medications available to help manage ET symptoms. It is important to work with your doctor to find a medication that is right for you. In addition, it is equally important to make sure that a high enough dose of medication is taken for it to be effective. Provided below is a list of common medications used for ET with upper limits of the dose by which we would expect an effect on tremor. If your physician has not prescribed doses of these medications similar to the ones listed, you may consider going back to your physician to try higher doses before considering other treatment options, such as deep brain stimulation. 

Doses of Essential Tremor Medications:

• Primidone – Up to 350 milligrams daily
• Propranolol  – Up to 320 milligrams daily
• Topiramate – Up to 400 milligrams daily
• Clonazepam – Up to 6 milligrams daily
• Gabapentin – Up to 2700 milligrams daily
• Mirtazepine – Up to 45 milligrams daily

Are there surgical options for essential tremor? 

Deep brain stimulation (DBS) is a therapeutic option for those with severe disabling ET not already managed by medications. DBS is often described as a pacemaker for the brain. It works much like a pacemaker, sending electrical signals to the brain instead of the heart. It is primarily utilized for patients who have Parkinson’s disease, dystonia, or essential tremor, who can’t adequately control their disease with medication.

Thalamotomy, involving the destruction of tremor producing cells in the brain region called the thalamus, is another surgical option. Using a small temperature-controlled electrode, a permanent lesion is created in the thalamus that helps to stop tremor without disrupting sensory or motor control.

Talk to your doctor about surgical and non-surgical options that are right for you.

Are there ways to treat essential tremor without medications?

Some patients may benefit from the Liftware device, which helps patients to eat with less spillage. This device comes with a stabilizing handle and a utensil attachment and works by stabilizing the utensil so that less food is spilled. Stress management and physical therapy are helpful for those with mild to moderate ET, but are typically used in combination with medications and/or surgery. For those with symptoms not controlled satisfactorily by medications, deep brain stimulation (DBS) or thalamotomy can be helpful in improving symptoms and may even help to reduce the amount of medications needed to improve symptoms. Your neurologist will be able to help you determine options that are right for you.

Is head tremor the same as essential tremor?

Head tremor is often described as an oscillation of the head, causing it to move side to side or up and down. The tremor can be rhythmic like a pendulum or irregular and more pronounced. While head tremors can be one of many types of tremors experienced by those with essential tremor, they are also seen in patients with dystonia. 

Can something be done about voice tremor?

Botulinum toxin injections are generally the most effective treatment for voice tremor. Deep brain stimulation (DBS) using bilateral stimulation (typically reserved for those with Parkinson’s disease or dystonia) may also help voice tremors, but will often cause slurred speech as well. For those with essential tremor, DBS is most often placed unilaterally (on one side of the brain), at least initially.

Sources:

Chou, K, Grube, S, Patil, P. Deep Brain Stimulation. A New Life for People with Parkinson’s Dystonia, and Essential Tremor. New York:  Demos Medical Publishing, 2012.
International Essential Tremor Foundation. (2010). ET vs. Parkinson’s: How do they differ? Retrieved January 15, 2015, from http://www.essentialtremor.org/wp-content/uploads/2013/07/ETvsPD092012.pdf National Institute of Neurological Disorders and Stroke. (July 24, 2014). Tremor Fact Sheet.  My head shakes:  is it dystonia? (2014).

Teaching Video NeuroImage: “Weighing” in on an Unusual Tremor

A 73-year-old right-handed man with hypertension, hypercholesterolemia, renal insufficiency, and cyclothymic disorder presented with 1 year of insidious onset tremor in his right hand when carrying his briefcase. Psychotropic drugs included bupropion and lamotrigine. He was neurologically intact except for a very low amplitude bilateral kinetic tremor (L > R) and a much larger amplitude right hand task-specific tremor (video 1) characterized by EMG (figure).

Video 1

Tremor phenomenology. There is a very low amplitude bilateral kinetic tremor, L>R. A more striking 6-Hz, moderate amplitude flexion-extension right hand tremor involving his wrist and metacarpophalangeal joints emerges when holding a bag. It disappears when the patient opens his hand or with fist clenching. A heavier load increases its amplitude.Download Supplementary Video 1 via http://dx.doi.org/10.1212/012141_Video_1

Figure Electrophysiologic Studies

Surface EMG recording of 6-Hz tremor in the right flexor carpi radialis and extensor carpi radialis muscles while holding a bag (weight ∼2.3 kg), with the hand in a “semi-opened” position. There was synchronous activation of agonist-antagonist muscles, which was specific to carrying weight in the right arm.

The phenomenology is classic for a weight-holding or “shopping bag tremor” first described in 1995.¹ It is difficult to categorize based on the consensus statement for tremor classification.² It could be considered a variant of isometric tremor, essential tremor, or task-specific tremor with different underlying etiologies. It is typically an asymmetric, progressive kinetic tremor that appears exclusively (or is more evident) when holding a weight, in contrast to classical essential tremor, which reduces in amplitude with weight-bearing.

Study Funding

No targeted funding reported.

Disclosure

M. Villa-López and O. Eungseok report no disclosures relevant to the manuscript. R. Chen serves as Editor-in-Chief of the Canadian Journal of Neurologic Sciences, received honorarium from Allergen, Merz, and Ipsen, consulted for NeuroQore, and received research support from the Canadian Institutes of Health Research, National Institute of Neurologic Disorders and Stroke, Canada Foundation for Innovation, Ontario Research Fund, National Science and Engineering Research Council of Canada, Dystonia Medical Research Foundation, Weston Brain Foundation, and National Organization for Rare Disease, outside the submitted work. A.E. Lang reports consultancy support from AbbVie, Acorda, AFFiRis, Biogen, Denali, Janssen, Intracellular, Kallyope, Lundbeck, Paladin, Retrophin, Roche, Sun Pharma, Theravance, and Corticobasal Degeneration Solutions; advisory board support form Jazz Pharma, PhotoPharmics, and Sunovion; other honoraria from Sun Pharma, AbbVie, Sunovion, American Academy of Neurology, and the International Parkinson and Movement Disorder Society; grants from Brain Canada, Canadian Institutes of Health Research, Corticobasal Degeneration Solutions, Edmond J. Safra Philanthropic Foundation, Michael J. Fox Foundation, the Ontario Brain Institute, Parkinson Foundation, Parkinson Canada, and W. Garfield Weston Foundation; and royalties from Elsevier, Saunders, Wiley-Blackwell, Johns Hopkins Press, and Cambridge University Press outside the submitted work. M. Masellis reports advisory board support from Arkuda Therapeutics, Ionis Pharmaceuticals, Alector Pharmaceuticals, Wave Life Sciences, and Biogen Canada; royalties from Henry Stewart Talks Ltd; and grants paid to the institution from Roche, Alector, Weston Brain Institute, Ontario Brain Institute, and the Canadian Institutes of Health Research outside the submitted work. J. Hopyan reports royalties from Elsevier outside the submitted work. Go to Neurology.org/N for full disclosures.

Acknowledgment

The authors thank the patient for participation.

Appendix Authors

Footnotes

• Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

• ↵* These authors participated equally as co–senior authors.

• Teaching slides http://links.lww.com/WNL/B398

• © 2021 American Academy of Neurology

Essential Tremor: Treatments | Stanford Health Care

How Is Essential Tremor Treated?

Medical treatments

Medical treatments include the use of different medications, such as:

·     Beta Blockers (propranolol)

·     Anticonvulsants (such as primidone, gabapentin, or topiramate)

·     Benzodiazepines (such as clonazepam or diazepam).

Some patients may benefit from local injections of botulinum toxin (BTX), which may help suppress the tremor.

Frequently, medication therapy cannot adequately control tremor or the person experiences intolerable side effects from the medications. In these circumstances, a person may consider a procedural therapy to treat their tremor.

Non-Invasive MR Guided Focused Ultrasound

Some patients may be suitable for MR Guided Focused Ultrasound (MRgFUS). During a single procedure, MR imaging precisely targets high intensity focused ultrasound waves through the intact skull to the ventral intermediate nucleus of the thalamus, an area of the brain that is thought to be responsible for causing tremors. MRgFUS treatment results in an immediate, significant, and durable reduction of tremor. This procedure is currently only being done to relieve tremor from one side of the body, typically in the dominant hand. 

Surgical treatments

The traditional surgical treatment for essential tremor is thalamic deep brain stimulation. This works especially well for limb tremors, although it is also sometimes helpful for head and vocal tremors. During this procedure, electrodes are implanted in the ventral intermediate nucleus of the thalamus, an area of the brain that is thought to be responsible for causing tremors. The electrodes are then connected via an extension to an implantable pulse generator that is placed under the skin near the patient’s collarbone. Electrical signals delivered to the thalamus work to suppress the tremor. This therapy has the advantage of being adjustable and reversible, and can be used to treat tremor on both sides of the body. Patients can usually come off or reduce their medications after this procedure.

How to do an electrophysiological study of tremor

https://doi.org/10.1016/j.cnp.2019.06.002Get rights and content

Highlights

•

An electrophysiological study of tremor can be helpful for the diagnosis.

•

A study of hand tremor can be done with surface EMG and an accelerometer.

•

Analysis in the frequency domain allows separating the different tremor components.

•

Coherence analysis shows whether there are one or more oscillators.

Abstract

The electrophysiological characterization of hand tremors is a useful method to complement the history and physical exam of tremor patients. Our article describes the methodology (recording, processing and interpretation) used in a diagnostic/phenotypic hand tremor study conducted in our lab at the Human Motor Control Section of the National Institute of Neurological Disorders and Stroke (NINDS), at the National Institutes of Health. The necessary equipment includes two one-axis accelerometers and four-channel electromyography (EMG). The hand tremor is recorded at rest, posture with and without weight loading, and during movement (kinetic). The recorded signals are analyzed in the time and frequency domains. The characterization of the dominant frequencies in the accelerometers and their relationship with the EMG frequencies are essential for the differential diagnosis of different tremor syndromes. We describe the electrophysiological characteristics of several tremor syndromes such as enhanced physiological tremor, essential tremor, Parkinson tremor, pharmacological-induced tremor, orthostatic tremor, and functional (psychogenic) tremor. Simplified guidance for adoption of tremor studies as a clinical tool in a movement disorders subspecialty clinic is provided.

Keywords

Tremor

Electrophysiology

EMG

Accelerometry

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90,000 Parkinson’s Disease – Official website of the Federal State Budgetary Healthcare Institution KB No. 85 FMBA of Russia

General Brief Information

Parkinson’s disease is a slowly progressive degenerative disease of the central nervous system, the main manifestations of which are such movement disorders as hypokinesia, muscle stiffness, resting tremor, postural disorders. In addition, with Parkinson’s disease, autonomic, affective and other disorders develop. Distinguish between true parkinsonism (Parkinson’s disease) and parkinsonism syndrome, which can accompany many neurological diseases (TBI, brain tumors, strokes, encephalitis, etc.)). If Parkinson’s disease is suspected, the patient needs to undergo electroencephalography, rheoencephalography, and MRI of the brain.

Symptoms

The main manifestations of Parkinson’s disease are considered to be tremors, hypokinesia, muscle rigidity and postural instability, as well as mental and autonomic disorders.

Tremor or tremor is the most obvious and pronounced symptom of the disease, which most often worries a person at rest, but it can also occur as a postural or intentional manifestation.The frequency of tremor in parkinsonism reaches 4-6 movements per second. The tremor usually begins with the distal part of either arm, and in the course of the progression spreads to the second arm and both legs. The movement of the patient’s fingers during tremors may resemble coin counting in appearance. Also, tremor can occur in the head area, expressed by “yes-yes” or “no-no” movements, trembling of the eyelids, jaw or tongue. Very rarely, the tremor in parkinsonism covers the body completely. Most often, it intensifies in exciting situations, usually it can be seen in the patient at rest, and when moving, the trembling subsides or disappears altogether.

Hypokinesia is understood as a decrease in the level of spontaneous movement activity, which results in the patient’s immobility for many hours.

There is stiffness in the human body, he can actively move only after some delay and then, with a slower pace (characterizes the resulting bradykinesia). A person’s steps become shallow, a puppet gait, while the feet are clearly parallel to each other. At the same time, the patient’s facial expression and gaze are frozen, there is a pronounced amimia, a smile, and a crying grimace appears on the face very slowly, inhibited.

A person often freezes in a mannequin pose. His speech is monotonous and gradually fades away. The handwriting becomes discontinuous and shallow, which characterizes the development of micrography. Also, as a manifestation of hypokinesia, oligokinesia and synkinesia can occur, that is, a reduction in the total number of movements and the disappearance of friendly movements in the patient, such as sweeping movements of the hands when walking, wrinkling of the forehead when looking up and other things. The patient can no longer perform parallel actions, all his movements become automatic.

The rigidity of muscle tissue is manifested by a uniform increase in the tone of the muscles of the plastic plan. In this case, the limbs freeze in a bent position or in a completely unbent state, which is a manifestation of plastic wax flexibility. If rigidity begins to prevail in some muscle groups, then a mannequin or supplicant pose occurs, in which a stoop is expressed, the head tilts forward, the arms are bent at the elbows and pressed against the body, and the legs are bent at the hip and knee joints.If you try to passively bend and unbend the wrist joints, forearms, then you can feel the steppedness of muscle tension or a symptom of a toothed wheel.

When the muscle tone changes, the limbs can no longer spontaneously return to their original position after any performed action. This characterizes the emergence of the Westphal phenomenon, when, with a sharp dorsal bend of the foot, it remains in this position for some time and does not unbend on its own.

In the later stages and stages of the disease, postural instability occurs.The patient in this situation cannot spontaneously overcome neither the inertia of rest, nor the inertia of movement. A person can hardly start to move, and once started, he can no longer stop. When moving forward, the body begins to outstrip the legs, the center of gravity in the body is disturbed, loss of stability occurs and the person falls. This symptomatology can disappear on its own after sleep or under the influence of other factors, but after some time it comes back again.

In addition to impaired motor activity in patients with Parkinson’s disease, mental and autonomic disorders are usually pronounced, and metabolism is impaired.As a result of these processes, the patient may experience obesity, exhaustion, and increase the secretory activity of the sebaceous, sweat and salivary glands.

Depending on the manifestations and symptoms of the disease, the pathology under consideration can be subdivided into:

• trembling form, which is very characteristic of tremor of the head, limbs, lower jaw with high or medium amplitude, as well as increased (sometimes normal) muscle tone;
• a trembling-rigid form, in which tremor occurs in the distal parts of the limbs and, in the course of the progress of the disease, stiffness during voluntary movements is added;
• akinetic-rigid form (the most unfavorable of all), in which the patient’s movement activity drops sharply, often reaching immobility, and muscle tone rises sharply, which threatens to develop muscle contracture;
• mixed form, in which all of the above forms can appear both together and flow into one another;
• an atypical form, which is characterized by synucleinpathy (dementia with Lewy bodies, idiopathic parkinsonism, and others) or taupathy (cortico-basal dementia, supranuclear paresis of the gaze, and others).

Each form of Parkinson’s disease, in addition to the difference in manifestations, may require specific therapy and patient care.

Causes of occurrence

The causes of Parkinson’s disease do not always provoke an immediate disease, more often, under their influence, Parkinson’s syndrome is formed, which responds well to treatment, in contrast to the main form of the disease. Among the main causes of Parkinson’s disease are:

• defeat by high doses of free radicals of black matter;
• highly toxic damage to the meninges, which can occur during periods of poisoning, with internal intoxication due to the release of toxins from the liver;
• heredity, which manifests itself in about 20% of cases of all diagnosed pathologies of this kind and has an indirect effect on the onset of the disease;
• genetic factor, in which the presence of modified genes in the genetic code provokes parkinsonism at a young age;
• lack of vitamin D, which is responsible for building protective barriers that prevent the penetration of free radicals and toxic substances into the body, the lack of which becomes especially noticeable in old age;
• inflammations provoked by a bacterial or viral infection, such as encephalitis and others;
• trauma to the human brain of various degrees of severity;
• high cholesterol, provoking atherosclerotic changes;
• degenerative brain processes due to impaired blood circulation.

All of the above factors can form the etiology of the disease, however, they are not stable in this matter and do not always provoke such processes.

The mechanism of development of the disease at the initial stage is characterized by a decrease in the production of dopamine, which provokes damage in the brain. Degeneratively modified parts of the brain begin to die, which leads to the characteristic symptoms of the disease. At the onset of the disease at a young age, it is worthwhile to understand that the cause of the processes is hereditary factors, and with a late start of the disease, in the overwhelming majority of cases, it is worth keeping in mind the mechanism of the development of pathology due to various external influences on the patient’s body.

Despite the fact that the obvious causes of Parkinson’s disease have not yet been identified, the ways of diagnosing and treating pathology have long been known, they are determined in each case individually and often help to maintain the patient’s condition at the proper level.

Diagnostics

Parkinson’s disease is more characteristic of an elderly person and is irreversible, however, diagnosis is necessary to maintain the patient’s normal level of life and the timely choice of appropriate treatment.Early diagnosis in this aspect plays a key role.

The diagnosis of Parkinson’s disease is easily made even on the basis of the external symptomatic manifestations of the disease. The difficulty lies in the fact that other neurological pathologies may have similar symptoms, therefore, doctors are in no hurry to rush to make a diagnosis without examinations. The more complete the picture of the course of the disease, the more effective the therapy will be and the longer the patient will live in normal health.

Still, the main method for diagnosing parkinsonism is the clinical picture of the disease.All data indicating the occurrence of this pathology, the specialist takes into account and considers in a complex. Also, topical diagnostics of Parkinson’s disease is often carried out, which is a comprehensive diagnosis, with the help of which the localization of an inflammatory focus in the region of the patient’s brain or a complex of such foci is easily determined. The basis for topical diagnosis is often the clinical picture of the disease. In addition, there are other methods for diagnosing parkinsonism, among which differential diagnostics and other techniques occupy an important place.

DIFFERENTIAL DIAGNOSTICS

Differential diagnosis of Parkinson’s disease means a very careful collection of clinical data and their study. The fact is that if there are no pronounced symptoms of parkinsonism in the patient’s history, then the diagnosis can become a whole problem for the doctor.

It is very important to differentiate the symptoms that are observed in the patient from the symptoms of prolonged depression, post-stroke state and other pathological conditions.

At the same time, it is important to understand that today in medicine there are no special tests that can be used to determine Parkinson’s disease. The importance of differential diagnosis is determined by the fact that it must be carried out regularly between courses of treatment in order to understand their effectiveness and promptly make competent adjustments to them.

DIAGNOSTICS OF DISEASE USING MRI

To confirm the diagnosis of parkinsonism at any stage of the disease, MRI of the patient’s brain can be performed, since the death of nerve cells during degenerative changes can be observed with its help.In their place, empty voids will be visible on the tomogram, which will be evidence of parkinsonism.

In addition to the fact that no dangerous X-rays are used in the MRI process, this examination is considered non-invasive, since during its course no human membranes are damaged. Magnetic resonance imaging is completely painless for humans. To make the MRI result more informative, during the diagnosis, special contrast agents are used, which are introduced into the body using intravenous injections.Contrasting greatly enhances the information content of the MRI scan, and on the basis of such data, an accurate diagnosis can be made and an effective treatment can be prescribed.

Treatment methods

For the effectiveness of the treatment of Parkinson’s disease, it is necessary to diagnose the disease in a timely manner and prescribe the appropriate therapy. Comprehensive treatment of this pathology implies a whole range of measures:

• the use of drug therapy, which, in addition to symptomatic drugs, must necessarily include the use of neuroprotective agents;
• the use of various folk remedies and methods of treatment;

90,037 rehabilitation procedures, including medical and social means;

• neurosurgical interventions.

Modern medicine understands the goal of treating Parkinson’s disease as two basic principles – preventing the development of pathology by stopping the process of degeneration of brain tissue and eliminating the symptoms of the disease, in which the patient begins to feel much better. Both of these goals should be achieved taking into account the degree of development of the disease in the patient.

90,000 April 11 – World Day Against Parkinson’s Disease (Zhukovskaya City Clinical Hospital)

Parkinson’s Disease is a chronic disease characteristic of people in the older age group.It is caused by the progressive destruction and death of neurons of the substantia nigra of the midbrain and other parts of the central nervous system, using dopamine as a neurotransmitter. the influence of the globus pallidum (pallidum), located in the anterior part of the brain, on the striatum (striatum).Damage to pallidum neurons leads to “inhibition of inhibition” of peripheral motor neurons (motoneurons of the spinal cord). At the moment, the disease is incurable, but the existing methods of conservative and surgical treatment can significantly improve the quality of life of patients. The disease owes its name to the French neurologist Jean Charcot. He suggested that it be named after James Parkinson, a British physician and author of Essays on Shaking Palsy, whose work was not properly appreciated during his lifetime.

Epidemiology Parkinson’s disease accounts for 75 – 80% of cases of Parkinson’s syndrome. It is the most common neurodegenerative disease after Alzheimer’s disease. The disease is ubiquitous. Its frequency ranges from 60 to 140 people per 100 thousand of the population, the number of patients increases significantly among representatives of the older age group. The proportion of people with Parkinson’s disease in the age group over 60 years old is 1%, and in the population over 85 years old – from 2.6% to 4%.Most often, the first symptoms of the disease appear at the age of 55-60. However, in some cases, the disease can develop before the age of 40 (early-onset Parkinson’s disease) or before the age of 20 (juvenile form of the disease). Men get sick more often than women. There were no significant racial differences in the morbidity structure.

Causes The etiology of Parkinson’s disease is not fully understood. Aging, genetic predisposition, exposure to environmental factors are considered etiological risk factors.Pathomorphologically normal aging is accompanied by a decrease in the number of neurons in the substantia nigra and the presence of Lewy bodies in them. Aging is also accompanied by neurochemical changes in the striatum – a decrease in the content of dopamine and the enzyme tyrosine hydroxylase, as well as a decrease in the number of dopamine receptors. Positron emission tomography has shown that the rate of degeneration of substantia nigra neurons in Parkinson’s disease is much higher than in normal aging. About 15% of people with Parkinson’s disease have a family history of the condition.However, the genes responsible for the development of Parkinson’s disease have not been identified.Parkinson-like manifestations can also be caused by environmental factors (pesticides, herbicides, heavy metal salts), chronic cerebrovascular insufficiency, or the use of drugs that cause extrapyramidal side effects.

Environmental factors It was found that after injection of the substance 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (eng. 1-methyl-4-phenyl-1,2,3,6 -tetrahydropyridine, abbr.MPTP) develops parkinsonism. MPTP penetrates the BBB and under the action of MAO-B is oxidized to 1-methyl-4-phenylpyridine (MPP +). MPP + penetrates into mitochondria and inhibits complex I of the respiratory chain. The similarity of the chemical structure of MPTP and some pesticides (for example, rotenone paraquat) and herbicides (for example, Agent Orange) suggested that MPTP-like environmental toxins contribute to the development of Parkinson’s disease. Risk factors also include living in rural areas and the proximity of industrial enterprises and quarries.The risk of developing Parkinson’s disease in smokers is 3 times lower than in nonsmokers. This is thought to be related to the dopamine-stimulating effect of nicotine. In addition, this can be explained by the presence of compounds in tobacco smoke, the action of which is similar to MAO inhibitors. The use of caffeine also protects against the development of Parkinson’s disease.

Pathological anatomy In Parkinson’s disease, the structures of the extrapyramidal system are affected – the basal nuclei and the black matter, the blue spot and others.The most pronounced changes are noted in the anterior sections of the substantia nigra. Symptoms characteristic of Parkinson’s disease occur when 60 – 80% of the neurons of this anatomical formation die. Macroscopic changes are characterized by depigmentation of melanin-containing areas of the black matter and blue spot. Microscopic examination of the affected areas reveals a decrease in the number of nerve cells. The presence of Levi’s bodies is determined in them. It also kills astrocytes (a type of glial cell) and activates microglia.Lewy bodies are formed due to the accumulation of the protein α-synuclein in the cytoplasm. The presence of Lewy bodies is one of the hallmarks of Parkinson’s disease. Lewy bodies are also found in other neurodegenerative diseases. As such, they are not considered a specific marker for Parkinson’s disease. Also, with this disease in the substantia nigra and blue spot, “pallid bodies” are found – intracellular granular inclusions that replace decaying melanin. According to the classification proposed by Braak et al., In the asymptomatic stage of Parkinson’s disease, Lewy bodies appear in the nerve cells of the olfactory bulb, medulla oblongata and pons varoli.With the progression of the disease, the presence of these pathological bodies is noted in the neurons of the substantia nigra, midbrain, basal ganglia, and at the final stages in the cells of the cerebral cortex.

Classification The most commonly used in medicine is the classification of the stages of parkinsonism according to Hyun and Yar. It was first published in 1967 in the journal Neurology by Margaret Hoehn and Yahr. She originally described 5 stages of Parkinson’s disease progression (1-5).Subsequently, the scale was modified by adding stages 0, 1.5 and 2.5.

Stage 0 – no signs of disease. Stage 1 – symptoms appear on one of the limbs; Stage 1.5 – symptoms appear on one of the limbs and trunk; Stage 2 – bilateral manifestations without postural instability. Stage 2.5 – bilateral manifestations with postural instability. The patient is able to overcome the inertia of movement caused by a push. Stage 3 – bilateral manifestations.Postural instability. The patient is capable of self-care. Stage 4 – immobility, need for outside help. In this case, the patient is able to walk and / or stand without support. Stage 5 – The patient is confined to a chair or bed. Severe disability.

There are several clinical forms of the disease: rigid-bradykinetic, trembling-rigid and trembling: the rigid-bradykinetic form is characterized by an increase in muscle tone according to the plastic type, a progressive slowdown of active movements up to immobility.Muscle contractures appear. Characteristic is the “pose of a mannequin” (“pose of the supplicant”).

o The trembling-rigid form is characterized by tremor of the extremities, mainly of their distal parts, to which the stiffness of voluntary movements is added.

o The trembling form is characterized by the presence of constant or almost constant medium and large-amplitude tremor of the extremities, tongue, head, lower jaw. Muscle tone is normal or slightly increased. The tempo of voluntary movements is saved.

Symptoms Parkinson’s disease is characterized by 4 movement disorders (tremor, hypokinesia, muscle rigidity, postural instability), as well as autonomic and mental disorders.

Tremor (tremor) is the most obvious and easily identifiable symptom. Parkinsonism is characterized by a tremor that occurs at rest, although other types (postural, intentional) are rarely possible. Its frequency is 4 – 6 Hz (movements per second). It usually begins in the distal part of one arm, spreading to the opposite arm and legs as the disease progresses.The multidirectional movements of the thumb and other fingers outwardly resemble counting coins or rolling pills (similar to the manual pill-making technique in pharmaceuticals). Sometimes there is also a “yes-yes” or “no-no” trembling of the head, trembling of the eyelids, tongue, lower jaw. In rare cases, it covers the whole body. The tremor increases with excitement and subsides with sleep and voluntary movements. Unlike cerebellar tremor, which appears during movement and is absent at rest, Parkinson’s disease is typically present at rest and decreases or disappears with movement.Hypokinesia is a decrease in spontaneous motor activity. The patient can freeze, remaining motionless for hours. General stiffness is characteristic. Active movements occur after some delay, their pace is slowed down – bradykinesia. The patient walks in small steps, while the feet are parallel to each other – a puppet gait. Mask-like face (amimia), fixed gaze, rare blinks. A smile, a grimace of crying appear with a delay and just as slowly disappear. Speech is devoid of expressiveness, monotonous and tends to fade.As a result of the decrease in the range of motion characteristic of Parkinson’s disease, the handwriting becomes small – micrography.

One of the manifestations of oligokinesia (decrease in the number of movements) is the absence of physiological synkinesis (friendly movements). When walking, the arms do not make the usual sweeping movements; they remain pressed to the body (acheirokinesis). When looking up, there is no wrinkling of the forehead. The clenching of the fingers into a fist is not accompanied by the extension of the hand. The patient cannot perform several targeted movements at the same time.All actions resemble automatic ones.

Muscle stiffness – uniform increase in muscle tone according to the plastic type. The limbs, when they bend and unbend, freeze in the position given to them. This form of muscle tone enhancement is called “plastic wax flexibility”. The predominance of rigidity in certain muscle groups leads to the formation of a characteristic pose of the supplicant (also called the “mannequin pose”): the patient slouches, the head is tilted forward, the arms bent at the elbow joints are pressed to the body, the legs are also slightly bent at the hip and knee joints.With passive flexion-extension of the forearm, head, circular movements in the wrist joint, you can feel a kind of discontinuity, graded muscle tension – a “cogwheel symptom.” Changes in muscle tone lead to a violation of the limb’s tendency to return to its original position after a perfect movement. For example, after a sharp passive dorsiflexion of the foot, it retains the position given to it for some time – the Westphal phenomenon.

Postural instability – develops in the late stages of the disease.The patient has difficulties in overcoming both rest inertia and movement inertia. It is difficult for the patient to start moving, and once it starts, it is difficult to stop. There are phenomena of propulsion (Latin propulsio – pushing forward), lateropulsions and retropulsion. They are expressed in the fact that, having begun to move forward, to the side or back, the body usually seems to be ahead of the legs, as a result of which the position of the center of gravity is disturbed. The person loses stability and falls. Sometimes patients have “paradoxical kinesias”, when, due to emotional experiences, after sleep, or due to other factors, a person begins to move freely, the symptoms characteristic of the disease disappear.Symptoms return after a few hours.

Autonomic and mental disorders In addition to disorders of the motor sphere, in Parkinson’s disease, vegetative disorders, as well as metabolic disorders, are noted. The consequence can be either wasting (cachexia) or obesity. Secretory disorders are manifested by greasy skin, especially the face, increased salivation, excessive sweating. Psychiatric disorders in Parkinson’s disease can be caused by both the disease itself and antiparkinsonian drugs.The initial signs of psychosis (fear, confusion, insomnia, hallucinatory-paranoid state with disorientation) are noted in 20% of outpatients and two-thirds of patients with severe parkinsonism. Dementia is less pronounced than in senile dementia. 47% have depression, 40% have sleep disorders and pathological fatigue. Patients are inactive, lethargic, and also annoying, prone to repeating the same questions. Due to the abundance and intensity of symptoms characteristic of Parkinson’s disease, its diagnosis in severe cases is not difficult.At the initial stages of the disease, when the manifestations of the disease are not expressed or are poorly expressed, the correct diagnosis can be facilitated by the identification of postural reflexes (reflexes of position). These include the Westphal phenomenon described above, as well as the Foie-Thévenard phenomenon (or the shin phenomenon). These reflexes arise due to an increase in the plastic tone of the muscles. The shin phenomenon is manifested by the fact that the patient’s leg, which is maximally bent at the knee joint, which lies on his stomach, descends slowly and usually does not fully unbend.

Diagnostics Diagnosis of Parkinson’s disease in most cases does not cause difficulties – it is enough for the patient to have hypokinesia and one of the symptoms: resting tremor, rigidity, postural disorders in combination with the positive effect of taking levodopa. The differential diagnosis of Parkinson’s disease with other pathologies takes place in two stages. Conditions and processes in which there are symptoms similar to parkinsonism should be excluded. If a patient has parkinsonism, it must be borne in mind that this syndrome is characteristic of a number of diseases.Symptoms pathognomonic for parkinsonism are observed when: psychomotor retardation – depression, catatonic stupor, hysteria, hypersomnia

o muscle hypertonicity – neuromyotonia, “rigid person” syndrome

o gait apraxia – normotensive hydrocephalus

brain tumors and other2 cerebellar damage

Parkinson’s disease can also be caused by a variety of diseases. In most cases (~ 80%) it is caused by damage to the nigrostriatal system due to Parkinson’s disease.With lesions of the corresponding parts of the central nervous system of a different etiology, toxic, medicinal, post-encephalitic, vascular, post-traumatic and other parkinsonisms will occur. In many diseases, Parkinson’s syndrome develops in combination with symptoms of damage to other parts of the central nervous system. The term “parkinson-plus” is used to refer to this group of diseases.

In 1992, the British physician Hughes proposed criteria for the diagnosis of Parkinson’s disease, allowing the diagnosis to be made with an accuracy of 93% (according to autopsy data):

1.the presence of hypokinesia and at least one of the following symptoms: rigidity, resting tremor 4 – 6 Hz, postural disturbances

2. persistent positive effect of levodopa

3. asymmetric onset of the disease (stage of hemiparkinsonism)

4. progressive course

5. no history of possible etiological factors of secondary parkinsonism (taking antipsychotics, reliably transferred encephalitis, acute cerebrovascular accident, repeated or severe traumatic brain injury)

a) the absence of the following symptoms at all stages of the disease

b) distinct pyramidal and / or symptoms

supranuclear gaze palsy

oculogyric crises

b) in the early stages of the disease

gross postural disorders

gross progressive autonomic insufficiency

· Severe dementia

These criteria should only be met when selecting patients for research.For a preliminary diagnosis, only the first two points are sufficient.

Treatment Conservative treatment. All existing treatments are aimed at relieving the symptoms of Parkinson’s disease (symptomatic treatment). The main drugs that eliminate movement disorders: levodopa (more often in combination with peripheral DOPA-decarboxylase inhibitors or less often with COMT inhibitors), dopamine receptor agonists and MAO-B inhibitors.

Dopaminergic drugs Dioxyphenylalanine (abbreviated dopa, or dopa) is a biogenic substance that is formed in the body from tyrosine and is a precursor of dopamine, which in turn is a precursor of norepinephrine.Due to the fact that in Parkinson’s disease the content of dopamine in the brain is significantly reduced, for the treatment of the disease it is advisable to use substances that increase its content in the central nervous system. Dopamine itself cannot be used for this purpose, since it poorly penetrates the blood-brain barrier.

Levodopa The synthetic levorotatory isomer of dioxyphenylalanine (abbreviated as L-dopa), which is much more active than dextrorotatory, is widely used as a drug.Levodopa is well absorbed when taken orally. Most of the drug enters the liver and is converted to dopamine, which does not cross the blood-brain barrier. To reduce decarboxylation, the drug is recommended to be used with dopa-decarboxylase inhibitors (benserazide, carbidopa). The drug is effective in Parkinson’s disease and parkinsonism. It reduces hypokinesia and rigidity. With tremor, dysphagia and salivation, the therapeutic effect is achieved in 50-60%. The drug can be prescribed with central anticholinergic blockers and should not be used with irreversible inhibitors of monoamine oxidase (MAO).When using, side effects are possible: dyspeptic phenomena (nausea, vomiting, loss of appetite), hypotension, arrhythmias, hyperkinesis, etc. In patients under 60 – 70 years old, the appointment of levodopa due to the development of side effects and a decrease in effectiveness with prolonged therapy is tried to be postponed and used other medicines. Treatment of patients over 70 years old, even in the initial stages, is recommended to start with levodopa, which is explained by the lower efficacy of drugs from other groups and more frequent somatic and mental side effects at this age.

Dopamine agonists Dopamine receptor agonists (bromocriptine, pergolide, pramipexole, ropinirole, cabergoline, apomorphine, lisuride) are also used as the main treatment. Drugs in this group are specific central dopamine receptor agonists. By mimicking the action of dopamine, they produce the same pharmacological effects as levodopa. Compared with levodopa, they are less likely to cause dyskinesias and other movement disorders, but more often have other side effects: edema, drowsiness, constipation, dizziness, hallucinations, and nausea.Inhibitors of monoamine oxidase type B (MAO-B) and catechol-O-methyltransferase (COMT) This group of drugs selectively inhibits the activity of enzymes that break down dopamine: MAO-B and COMT. Selegiline (MAO-B inhibitor), entacapone and tolcapone (COMT inhibitors) slow the steady progression of Parkinson’s disease. Pharmacological effects are similar to those of levodopa, although their severity is much less. They allow you to enhance the effects of levodopa without increasing or even decreasing its total dose. Inhibitors of neuronal reuptake of dopamine

Indirect dopaminomimetics (amantadine, gludantan) increase the sensitivity of receptors to the corresponding mediator.These drugs increase the release of dopamine from presynaptic terminals and inhibit its reverse neuronal uptake. Medicines of this group cause the same pharmacological effects as levodopa, that is, they mainly suppress hypokinesia and muscle rigidity, significantly less affecting tremor.

Central anticholinergics Anticholinergics are used to treat parkinsonism. The famous French physician Jean Charcot used belladonna as early as 1874 to reduce the increased salivation observed in the disease.They also noted a decrease in tremor when taking it. In the future, not only belladonna preparations began to be used for treatment, but also other anticholinergic antagonists – atropine and scopolamine. After the appearance of synthetic anticholinergics, trihexyphenidil (cyclodol), triperidene, biperidene, tropacin, etpenal, didepil and dinesin began to be used. The use of anticholinergics is pathogenetically justified. Damage to the substantia nigra and other nerve formations leads to significant shifts in choline and dopaminergic processes, namely, an increase in cholinergic activity and a decrease in dopaminergic activity.Thus, the central anticholinergic antagonists “align” neurotransmitter interactions.

Previously used belladonna preparations act mainly on peripheral acetylcholine receptors and less on cholinergic receptors in the brain. In this regard, the therapeutic effect of these drugs is relatively small. Along with this, they cause a number of side effects: dry mouth, impaired accommodation, urinary retention, general weakness, dizziness, etc. Modern synthetic antiparkinsonian central anticholinergics are characterized by a more selective effect.They are widely used in the treatment of extrapyramidal diseases, as well as neurological complications caused by neuroleptics. A distinctive feature of central anticholinergic antagonists is that they have a greater effect on tremors; to a lesser extent affect rigidity and bradykinesia. Due to the peripheral effect, salivation decreases, to a lesser extent sweating and greasiness of the skin.

Surgical treatment Surgical treatment methods can be divided into two types: destructive operations and stimulation of deep brain structures.Destructive operations To destructive operations used in Parkinson’s disease include thalomo – and pallidotomy. Thalamotomy is indicated only in cases where tremor is the main symptom of the disease. To obtain a positive result from the operation, patients must meet several criteria: Parkinson’s disease is manifested by unilateral tremor, conservative treatment is ineffective. It has been shown that the destruction of the ventral intermediate nucleus of the thalamus (Latin nucleus ventralis intramedius) leads to a decrease in tremor in patients with parkinsonism.According to the literature, the effectiveness of surgery to eliminate tremor in Parkinson’s disease reaches 96%. At the same time, the same authors note a high risk of complications (13% persistent and 56% transient). Complications arising after thalamotomy include dysarthria, abulia, dysphasia, dyspraxia. Pallidotomy can be indicated in patients with a predominance of movement disorders, for which conservative treatment is ineffective. The procedure consists in the introduction of a needle into the pallidum (Latin globus pallidus), followed by its partial destruction.Pallidotomy is a relatively safe procedure. When analyzing 85 articles devoted to pallidotomy, and, accordingly, the results of treatment of 1510 patients, the following complications of this operation were identified: Complication: Intracranial hemorrhage, postoperative psychosis, hypersalivation

What is paresis and how to treat it: causes and treatment

Paresis is a symptom, manifestation which is associated with pathologies in the body, such as a tumor of the brain or spinal cord, stroke, encephalitis, poliomyelitis, as well as processes that cause the destruction of the protein responsible for the transmission of nerve impulses.Paresis can result from encephalitis, multiple sclerosis, traumatic brain injury, and spinal injury.

Paresis are central (at the level of the brain and spinal cord) and peripheral (at the level of peripheral nerves). Central paresis is characterized by an increase in the tone of the affected muscles. Peripheral paresis develops in a group of muscles associated with the damaged nerve, and is expressed in muscle weakness and involuntary muscle twitching.

Paresis can affect either one side of the body (paresis of the arm and leg on one side), or both limbs (arms or legs at the same time, for example, paresis / paraparesis of the lower extremities), or one arm or leg (paresis of the arm or paresis of the leg).Most often, patients are faced with the manifestation of hemiparesis – paresis of one half of the body. With hemiparesis, the patient is worried about a decrease in skin sensitivity, soreness and swelling of muscles, weakness, impaired flexion and extension of the joint, tremors, unsteadiness of gait, uncoordinated movements. Right-sided hemiparesis occurs in patients much more often than left-sided. These patients often have difficulty reading, writing, counting.

In patients after trauma of the larynx, surgery on the organs of the neck (thyroid gland, carotid artery, cervical spine), with cancer, laryngeal paresis may occur – a temporary violation of the mobility of the muscles of the larynx.This diagnosis is established in patients with a disease duration of up to 6 months. The clinical guidelines of the Ministry of Health say that it is possible to restore the mobility of the muscles of the larynx in a period of several months to two years.

After a stroke, paresis of the facial nerve may occur. With paresis, the following is observed: drooping of the corner of the mouth, violation of the act of swallowing, limitation of the mobility of the eyebrow, inability to completely close the eye, violation of facial expressions. According to the WHO, damage to the facial nerve ranks second in frequency among diseases of the peripheral nervous system.Paresis of facial muscles leads not only to cosmetic defects and painful experiences of the patient, but also to impaired swallowing and chewing functions, impaired pronunciation and even loss of vision (when neuroparalytic keratitis is detected).

Parkinson’s disease. Center for Extrapyramidal Diseases

Parkinson’s Disease. Center for Extrapyramidal Diseases – Clinical presentation of Parkinson’s disease

Clinical manifestations of Parkinson’s disease

• Tremor. For Parkinson’s disease is characterized by a resting tremor of the type of “rolling pills” or “counting coins”. Most often, the tremor initially appears in the hand, but can begin in the leg, face, lower jaw, or tongue. In most cases, as the disease progresses, thermor sequentially involves parts of the body in the following order: 1-arm, 2-arm and leg on the same side, 3-opposite half of the body. With voluntary movement of the involved limb, the tremor disappears or is significantly weakened.When performing repetitive movements of the opposite limb, the tremor, on the contrary, intensifies. In addition, resting tremors in the hands are aggravated by walking.

• Postural kinetic tremor. In a significant part of patients with Parkinson’s disease , in addition to resting tremor, postural-kinetic thermor also occurs, which occurs or intensifies when holding a posture or movement. In some cases, such a tremor is a kind of “continuation” of the resting tremor and has the same frequency.In other patients, this is an independent type of tremor, which limits hand movements to a greater extent than resting tremor. It can make eating, dressing, and other activities involving delicate movements or the need to maintain a certain posture difficult.

• Hypokinesia is one of the most disabling manifestations of Parkinson’s disease . It is characterized by slowness of movements and obstructed initiation, depletion of the pattern, exhaustion of movements.The patient may describe hypokinesia as fatigue or clumsiness, awkwardness, and note that daily activities, such as dressing or eating, have become more time-consuming than usual. The performance of fine movements of the limbs suffers the most: patients cannot fasten buttons, writing is at a loss. When writing, the patient begins a line with relatively large letters, but towards the end of the line they become smaller and smaller (micrograph). As the disease progresses, other movements become more difficult.Many people complain that it is difficult for them to get up and out of the car, and also to perform movements that require mobility of the trunk or the maintenance of a difficult posture. In extreme cases, these changes can lead to limited mobility and even complete inability to move. Desiring to make a movement, patients can freeze in a certain position.

• Rigidity is manifested by an increase in resistance when performing passive movements with the involved limb.It is felt both when flexing and extending. In contrast to spasticity, rigidity is present throughout the entire range of motion: from its beginning to its end. Symptoms spread from the proximal to the distal, i.e. the first and most severely affected muscles are those that drive the large proximal joints.

• Postural instability manifests itself in the late stages Parkinson’s disease , on average about 5 years after its onset.This symptom leads to severe functional impairments and is practically not amenable to treatment. One of the reasons is an increase in the tone of the muscles of the trunk, especially the flexors, which leads to a constant tilt of the trunk forward. Patients often collapse due to their inability to quickly regain their balance. Often there is a need to use a cane, walker or ask someone to accompany them, which leads to a pronounced limitation of the independence of patients.

• Difficulty moving and walking disorders appear in the late stages Parkinson’s disease .Walking disorders increase slowly, while at first there is difficulty in tearing the foot off the floor and limitation of swinging the arms when walking. as the disease progresses, patients notice difficulty in starting movement, a mincing gait appears. It is characterized by a small, fast, uncontrolled step with the inability to stop. A mincing gait usually occurs when moving on a flat surface, but there is no difficulty in climbing stairs. At the moment of the beginning of movement, before a turn, when passing through a narrow opening (corridor, door), the unexpected appearance of an obstacle, a patient with Parkinson’s disease may suddenly freeze.

• Urinary disorders. Patients with Parkinson’s disease often have urinary disorders such as increased urination (pollakiuria), increased frequency of urination at night (nocturia), or urgency. A possible cause of these disorders is detrusor hyperreflexia and bladder overactivity.

• Urinary incontinence. In the late stages Parkinson’s disease urinary incontinence may occur, accompanied by bowel dysfunction such as constipation or pseudo-obstruction. These symptoms occur due to damage to the autonomic nervous system, however, pathogenesis remains unclear. The development of these symptoms is associated with the presence of Lewy bodies in the neurons of the sympathetic ganglia and the hypothalamus.

• Depression . 20-40% with Parkinson’s disease develop depression during the course of the disease.In 20-30%, it is the first symptom, ahead of movement disorders. One of the causes of depression is the weakening of the activity of the dopaminergic mesolimbic system, but lesions of the noradrenergic and serotonergic systems also play a role in its development.

• Alarms . Approximately 50% of patients with Parkinson’s disease develop anxiety, mainly in the form of panic attacks. Often, anxiety states are associated with motor fluctuations, arising during the “off” period.

• Dementia (dementia) develops in 15-30% of patients with Parkinson’s disease , in patients over 80 years old this figure can reach 70-80%. dementia is not a favorable prognostic factor, indicating the rapid progression of the disease. Risk factors for dementia: advanced age, low sensitivity to levodopa, akinetic-rigid form of the disease, the presence of psychotic episodes against the background of antiparkinsonian therapy, the presence of dementia in relatives.Typical symptoms: memory loss, impaired attention, mental retardation, impaired visual-spatial functions. The mechanisms of the development of dementia remain completely unclear, but autopsy data indicate the role of degenerative pathology with the formation of Lewy bodies and the deposition of amyloid in the limbic structures and cerebral cortex, as well as the weakening of the activity of the cholinergic system.

• Sleep disorders .Most patients with Parkinson’s disease have sleep disorders, mainly related to sleep maintenance. Sleep becomes intermittent and incomplete, does not bring a feeling of freshness. Falling asleep is also often disturbed. In the later stages of the disease, there is increased daytime sleepiness, accompanied by sudden fits of sleep. The most common parasomnias are nightmares, vivid dreams, night fears, miscarriage, sleepwalking. Particularly characteristic is disturbance in sleep behavior with rapid eye movements, in which muscle atony is lost in this phase of sleep and the patient begins to respond to dreams.Sometimes this disorder is many years ahead of other symptoms of Parkinson’s disease. In some people, restless legs syndrome causes difficulty falling asleep. Although there are many underlying causes of these disorders, the main cause is damage to the centers of the brain that regulate sleep.

90,000 Parkinson’s Disease – Neurovitis Clinic

Parkinson’s disease (synonyms: idiopathic parkinsonism syndrome, tremor palsy) is a slowly progressive chronic neurological disease characteristic of older people.Refers to degenerative diseases of the extrapyramidal motor system. It is caused by the progressive destruction and death of neurons that produce the neurotransmitter dopamine, primarily in the substantia nigra, as well as in other parts of the central nervous system. Insufficient dopamine production leads to an activating effect of the basal ganglia on the cerebral cortex.

The leading symptoms (otherwise: basic or cardinal symptoms) are:

– muscle stiffness

– hypokinesia

– tremor

– postural instability

Modern medicine cannot yet cure the disease or slow down its progression (etiological or pathogenetic therapy), but the existing methods of conservative and surgical treatment can significantly improve the quality of life of patients.

The term “parkinsonism” is a general concept for a number of diseases and conditions with the above-mentioned leading symptoms. However, the most significant form of parkinsonism is Parkinson’s disease – an idiopathic disease (which means an independent disease, not caused by genetic disorders or other diseases).

Epidemiology.

Parkinson’s disease accounts for 70-80% of cases of Parkinson’s syndrome. It is the most common neurodegenerative disease after Alzheimer’s disease.The disease is ubiquitous. Its frequency ranges from 60 to 140 people per 100 thousand of the population, the number of patients increases significantly among representatives of the older age group. The proportion of people with Parkinson’s disease in the age group over 60 years old is 1%, and over 85 years old – from 2.6% to 4%. Most often, the first symptoms of the disease appear in 55-60 years. However, in some cases, the disease can develop before the age of 40 (early-onset Parkinson’s disease) or up to 20 years (juvenile form of the disease).

Men get sick more often than women. There were no significant racial differences in the morbidity structure.

Etiology.

The etiology of Parkinson’s disease in the second half of 2011 has not been finally clarified. Aging, genetic predisposition, exposure to environmental factors are considered etiological risk factors. Pathomorphologically normal aging is accompanied by a decrease in the number of neurons in the substantia nigra and the presence of Lewy bodies in them.Aging is also accompanied by neurochemical changes in the striatum – a decrease in the content of dopamine and the enzyme tyrosine hydroxylase, as well as a decrease in the number of dopamine receptors. Positron emission tomography has shown that the rate of degeneration of substantia nigra neurons in Parkinson’s disease is much higher than in normal aging.

About 15% of people with Parkinson’s disease have a family history of the disease. However, the genes responsible for the development of Parkinson’s disease have not been identified.

The causes of parkinson-like manifestations can also be the effect of environmental factors (pesticides, herbicides, salts of heavy metals), chronic cerebrovascular insufficiency or the use of drugs that cause extrapyramidal side effects.

Environmental factors.

It was established that after injection of the substance 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), parkinsonism develops. MPTP penetrates the BBB and under the action of MAO-B is oxidized to 1-methyl-4-phenylpyridine (MPP +).MPP + penetrates into mitochondria and inhibits complex I of the respiratory chain. The similarity of the chemical structure of MPTP and some pesticides (eg, rotenone, paraquat) and herbicides (eg, Agent Orange) suggested that MPTP-like environmental toxins contribute to the development of Parkinson’s disease. Risk factors also include living in rural areas and the proximity of industrial enterprises and quarries.

The risk of developing Parkinson’s disease in smokers is 3 times lower than in nonsmokers.This is thought to be related to the dopamine-stimulating effect of nicotine. In addition, this can be explained by the presence of compounds in tobacco smoke, the action of which is similar to MAO inhibitors. The use of caffeine also protects against the development of Parkinson’s disease.

Oxidative hypothesis.

The oxidative hypothesis suggests that free radicals generated during the oxidative metabolism of dopamine play an important role in the development and progression of Parkinson’s disease. The content of substances that can serve as an electron donor in the black matter increases, which contributes to the formation of free radicals [2].In addition, when dopamine is oxidized by MAO, hydrogen peroxide is formed. If hydrogen peroxide does not bind to glutathione, then there is an accumulation of highly reactive hydroxyl radicals, which react with lipids of cell membranes, causing lipid peroxidation and cell death.

Pathogenesis

Pathological anatomy.

In Parkinson’s disease, the structures of the extrapyramidal system are affected – the basal nuclei and the substantia nigra, the blue spot and others.The most pronounced changes are noted in the anterior sections of the substantia nigra. Symptoms characteristic of Parkinson’s disease occur when 60-80% of the neurons of a given anatomical formation die.

Macroscopic changes are characterized by depigmentation of melanin-containing areas of the black matter and blue spot. Microscopic examination of the affected areas reveals a decrease in the number of nerve cells. The presence of Levi’s bodies is determined in them. It also kills astrocytes (a type of glial cell) and activates microglia.Lewy bodies are formed due to the accumulation of β-synuclein protein in the cytoplasm. The presence of Lewy bodies is one of the hallmarks of Parkinson’s disease.

Lewy bodies are also found in other neurodegenerative diseases. As such, they are not considered a specific marker for Parkinson’s disease. In addition, with this disease in the substantia nigra and blue spot, “pallid bodies” are found – intracellular granular inclusions that replace decaying melanin.

Pathological physiology.

A close relationship between the components of the extrapyramidal system – the pallidum and the striatum – is provided by numerous bundles of nerve fibers. Thanks to the connections between the thalamus and the striopallidal system, reflex arcs are formed, which ensure the execution of numerous stereotyped and automated movements (for example, walking, running, swimming, cycling, etc.). The close connection of the striopallidal system with the nuclei of the hypothalamus determines its role in the mechanisms of emotional reactions.Normally, the extrapyramidal system sends impulses to peripheral motor neurons. These signals play an important role in providing myostatics by making muscles ready for voluntary movements. The ability of a person to take an optimal posture for the intended action depends on the activity of this department of the central nervous system, the necessary ratio of the tone of the agonist and antagonist muscles, as well as the smoothness and proportionality of voluntary movements in time and space, is achieved.

The nature of the clinical manifestations of the disease depends on which part of the striopallidal system is affected – the striatum or pallidum.If the striatum has an excessively inhibitory effect, hypokinesia occurs – poor movement, amimia. The hypofunction of the striatum leads to the occurrence of excessive involuntary movements – hyperkinesis. Pallidum has an inhibitory effect on the structures of the striatum. Parkinson’s disease is characterized by a decrease in the inhibitory effect of pallidum on the striatum. Damage to the pallidum leads to “inhibition of inhibition” of peripheral motor neurons.

The discovery of the role of neurotransmitters made it possible to explain the functions of the extrapyramidal system, as well as the causes of the clinical manifestations of Parkinson’s disease and parkinsonism.There are several dopaminergic systems in the brain. One of them begins in the neurons of the substantia nigra, the axons of which, through the brain stem, the inner capsule, the pallidum, reach the striatum (lat.corpus striatum). The terminal sections of these axons contain large amounts of dopamine and its derivatives. Degeneration of this nigrostriatal dopaminergic pathway is the main causative factor in the development of Parkinson’s disease. The second ascending dopaminergic system is the mesolimbic pathway.It starts from the cells of the interpeduncular nucleus of the midbrain and ends in the hypothalamus and frontal lobes of the brain. This pathway takes part in the control of mood, behavior and controls the onset of the motor act and the movements of the affective reaction (movements that accompany emotions).

The basis of all forms of parkinsonism is a sharp decrease in the amount of dopamine in the substantia nigra and striatum and, accordingly, a disruption in the functioning of the dopaminergic pathways of the brain.The clinical picture. Parkinson’s disease is characterized by 4 movement disorders (tremor, hypokinesia, muscle rigidity, postural instability), as well as autonomic and mental disorders. Tremor (trembling) is the most obvious and easily identifiable symptom. Parkinsonism is characterized by tremor that occurs at rest, although other types (postural, intentional) are rarely possible. Its frequency is 4-6 Hz (movements per second). It usually begins in the distal part of one arm, spreading to the opposite arm and legs as the disease progresses.The multidirectional movements of the thumb and other fingers outwardly resemble counting coins or rolling pills (similar to the manual pill-making technique in pharmaceuticals). Sometimes there is also a “yes-yes” or “no-no” trembling of the head, trembling of the eyelids, tongue, lower jaw. In rare cases, it covers the whole body. The tremor increases with excitement and subsides with sleep and voluntary movements. Unlike cerebellar tremor, which appears during movement and is absent at rest, Parkinson’s disease is typically present at rest and decreases or disappears with movement.

Handwriting in Parkinson’s disease.

The figure shows jagged movements where smooth lines are assumed

Hypokinesia – decrease in spontaneous motor activity. The patient can freeze, remaining motionless for hours. General stiffness is characteristic. Active movements occur after some delay, their pace is slowed down – bradykinesia. The patient walks in small steps, while the feet are parallel to each other – a puppet gait.Mask-like face (amimia), fixed gaze, rare blinks. A smile, a grimace of crying appear with a delay and just as slowly disappear.

Speech lacks expression, is monotonous and tends to fade. As a result of the decrease in the range of motion characteristic of Parkinson’s disease, the handwriting becomes small – micrography.

One of the manifestations of oligokinesia (decrease in the number of movements) is the absence of physiological synkinesis (friendly movements).When walking, the arms do not make the usual sweeping movements; they remain pressed to the body (acheirokinesis). When looking up, there is no wrinkling of the forehead. The clenching of the fingers into a fist is not accompanied by the extension of the hand. The patient cannot perform several targeted movements at the same time. All actions resemble automatic ones.

Muscle stiffness – uniform increase in muscle tone according to the plastic type. The limbs, when they bend and unbend, freeze in the position given to them.This form of muscle tone enhancement is called “plastic wax flexibility”. The predominance of rigidity in certain muscle groups leads to the formation of a characteristic pose of the supplicant (also called the “mannequin pose”): the patient slouches, the head is tilted forward, the arms bent at the elbow joints are pressed to the body, the legs are also slightly bent at the hip and knee joints. With passive flexion-extension of the forearm, head, circular movements in the wrist joint, one can feel a kind of discontinuity, graded muscle tension – a “symptom of a cogwheel.”
Changes in muscle tone lead to disruption of the limb’s tendency to return to its original position after a perfect movement. For example, after a sharp passive dorsiflexion of the foot, it retains the position given to it for some time – the Westphal phenomenon.

Postural instability develops in the later stages of the disease. The patient has difficulties in overcoming both rest inertia and movement inertia. It is difficult for the patient to start moving, and once it starts, it is difficult to stop.There are phenomena of propulsion (Latin propulsio – pushing forward), lateropulsions and retropulsion. They are expressed in the fact that, having begun to move forward, to the side or back, the body usually seems to be ahead of the legs, as a result of which the position of the center of gravity is disturbed. The person loses stability and falls. Sometimes patients have “paradoxical kinesias”, when, due to emotional experiences, after sleep, or due to other factors, a person begins to move freely, the symptoms characteristic of the disease disappear.Symptoms return after a few hours.

Autonomic and mental disorders.

In addition to disorders of the motor sphere, autonomic disorders, as well as metabolic disorders, are noted in Parkinson’s disease. The consequence can be either wasting (cachexia) or obesity. Secretory disorders are manifested by greasy skin, especially the face, increased salivation, excessive sweating.

Mental disorders in Parkinson’s disease can be caused both by the disease itself and by antiparkinsonian drugs.The initial signs of psychosis (fear, confusion, insomnia, hallucinatory-paranoid state with disorientation) are noted in 20% of outpatients and two-thirds of patients with severe parkinsonism. Dementia is less pronounced than in senile dementia. 47% have depression, 40% have sleep disorders and pathological fatigue. Patients are inactive, lethargic, and also annoying, prone to repeating the same questions.

There are several clinical forms of the disease – rigid-bradykinetic, trembling-rigid and trembling:

• The rigid-bradykinetic form is characterized by an increase in muscle tone according to the plastic type, a progressive slowdown in active movements up to immobility.Muscle contractures appear. Characteristic is the “pose of a mannequin” (“pose of the supplicant”).
• The trembling-rigid form is characterized by tremor of the limbs, mainly of their distal parts, to which the stiffness of voluntary movements is added.
• The trembling form is characterized by the presence of a constant or almost constant medium and large-amplitude tremor of the limbs, tongue, head, and lower jaw. Muscle tone is normal or slightly increased. The tempo of voluntary movements is saved.

90 100 Hyun and Yar stages of parkinsonism (Hoehn, Yahr, 1967)

The most commonly used in medicine is the classification of the stages of parkinsonism according to Hyun and Yar. It was first published in 1967 in the journal Neurology by Margaret Hoehn and Yahr. She originally described 5 stages of Parkinson’s disease progression (1-5). Subsequently, the scale was modified by adding stages 0, 1.5 and 2.5.

• Stage 0 – no signs of disease.
• Stage 1 – Symptoms appear on one of the limbs.
• Stage 1.5 – Symptoms appear on one of the limbs and trunk.
• Stage 2 – bilateral manifestations without postural instability.
• Stage 2.5 – bilateral manifestations with postural instability. The patient is able to overcome the inertia of movement caused by a push.
• Stage 3 – bilateral manifestations. Postural instability. The patient is capable of self-care.
• Stage 4 – immobility, need for outside help. In this case, the patient is able to walk and / or stand without support.
• Stage 5 – The patient is confined to a chair or bed. Severe disability.

Treatment

Conservative treatment.

Currently, Parkinson’s disease is incurable, all existing methods of treatment are aimed at alleviating its symptoms (symptomatic treatment).

The main drugs that eliminate movement disorders: levodopa (more often in combination with peripheral DOPA-decarboxylase inhibitors or less often with COMT inhibitors), dopamine receptor agonists [en] and MAO-B inhibitors.

Dopaminergic drugs.

Dioxyphenylalanine (abbreviated as dopa, or dopa) is a biogenic substance that is formed in the body from tyrosine and is a precursor of dopamine, which in turn is a precursor of norepinephrine.Due to the fact that in Parkinson’s disease the content of dopamine in the brain is significantly reduced, for the treatment of the disease it is advisable to use substances that increase its content in the central nervous system. Dopamine itself cannot be used for this purpose, since it poorly penetrates the blood-brain barrier.

Levodopa.

The synthetic levorotatory isomer of dioxyphenylalanine (abbreviated as L-dopa), which is much more active than dextrorotatory, is widely used as a drug.Levodopa is well absorbed when taken orally. Most of the drug enters the liver and is converted into dopamine, which does not cross the blood-brain barrier. To reduce decarboxylation, the drug is recommended to be used with dopa-decarboxylase inhibitors (benserazide, carbidopa).

The drug is effective against Parkinson’s disease and parkinsonism. It reduces hypokinesia and rigidity. With tremor, dysphagia and salivation, the therapeutic effect is achieved in 50-60%.

The drug can be administered with central anticholinergics and should not be used with irreversible inhibitors of monoamine oxidase (MAO).

When applied, side effects are possible: dyspeptic symptoms (nausea, vomiting, loss of appetite), hypotension, arrhythmias, hyperkinesis, etc.

In patients under 60-70 years of age, the appointment of levodopa due to the development of side effects and a decrease in effectiveness with prolonged therapy is trying to be postponed and other drugs are used. Treatment of patients over 70 years old, even in the initial stages, is recommended to start with levodopa, which is explained by the lower efficacy of drugs from other groups and more frequent somatic and mental side effects at this age.

Dopamine agonists.

Dopamine receptor agonists (bromocriptine, pergolide, pramipexole, ropinirole, cabergoline, apomorphine, lisuride) are also used as the main treatment. Drugs in this group are specific central dopamine receptor agonists. By mimicking the action of dopamine, they produce the same pharmacological effects as levodopa.

Compared with levodopa, they are less likely to cause dyskinesias and other movement disorders, but more often have other side effects: edema, drowsiness, constipation, dizziness, hallucinations, and nausea.Inhibitors of MAO type B and catechol-O-methyltransferase.

This group of drugs selectively inhibits the activity of enzymes that break down dopamine: monoamine oxidase (MAO type B) and catechol-O-methyltransferase (COMT). MAO-B inhibitors (eg selegiline, rasagiline] and COMT inhibitors (eg entacapone and tolcapone) slow the steady progression of Parkinson’s disease. Pharmacological effects are similar to those of levodopa, although their severity is significantly less. They can enhance the effects of levodopa without increasing or even reducing it total dose.

Dopamine reuptake inhibitors

Indirect dopaminomimetics (amantadine, gludantan) increase the sensitivity of receptors to the corresponding mediator. These drugs increase the release of dopamine from presynaptic terminals and inhibit its reverse neuronal uptake. Medicines of this group cause the same pharmacological effects as levodopa, that is, they mainly suppress hypokinesia and muscle rigidity, significantly less affecting tremor.

Central holinoblockers

Trihexyphenidyl – the main drug of the group of central anticholinergic antagonists used to treat Parkinson’s disease

Anticholinergics are used to treat parkinsonism. The famous French physician Jean Charcot used belladonna as early as 1874 to reduce the increased salivation observed in the disease. They also noted a decrease in tremor when taking it. In the future, not only belladonna preparations began to be used for treatment, but also other anticholinergic blockers – atropine and scopolamine.After the appearance of synthetic anticholinergics, trihexyphenidil (cyclodol), triperidene, biperidene, tropacin, etpenal, didepil and dinesin began to be used. The use of anticholinergics is pathogenetically substantiated. Damage to the substantia nigra and other nerve formations leads to significant shifts in choline and dopaminergic processes, namely, an increase in cholinergic activity and a decrease in dopaminergic activity. Thus, the central anticholinergic antagonists “align” neurotransmitter interactions.

Previously used belladonna preparations act mainly on peripheral acetylcholine receptors and less on cholinergic receptors in the brain. In this regard, the therapeutic effect of these drugs is relatively small. Along with this, they cause a number of side effects: dry mouth, impaired accommodation, urinary retention, general weakness, dizziness, etc. Modern synthetic antiparkinsonian central anticholinergics are characterized by a more selective effect.They are widely used in the treatment of extrapyramidal diseases, as well as neurological complications caused by neuroleptics. A distinctive feature of central anticholinergic antagonists is that they have a greater effect on tremor; to a lesser extent affect rigidity and bradykinesia. Due to the peripheral effect, salivation decreases, to a lesser extent sweating and greasiness of the skin.

Surgical treatment.

Surgical methods of treatment can be divided into two types : destructive operations and stimulation of deep brain structures.

Destructive operations

The destructive operations used in Parkinson’s disease include thalomo- and pallidotomy.

Thalamotomy is indicated only in cases where the main symptom of the disease is tremor. To obtain a positive result from the operation, patients must meet several criteria: Parkinson’s disease is manifested by unilateral tremor, conservative treatment is ineffective. It has been shown that the destruction of the ventral intermediate nucleus of the thalamus (lat.nucleus ventralis intramedius) leads to a decrease in tremor in patients with parkinsonism. According to the literature, the effectiveness of surgery to eliminate tremor in Parkinson’s disease reaches 96%. At the same time, the same authors note a high risk of complications (up to 1/6 – persistent and about 1/2 – transient).

Complications after thalamotomy include dysarthria, abulia, dysphasia, dyspraxia.

Pallidotomy can be indicated in patients with predominance of movement disorders, for whom conservative treatment is ineffective.The procedure consists in the introduction of a needle into the pallidum (Latin globus pallidus), followed by its partial destruction.

Pallidotomy is a relatively safe procedure. When analyzing 85 articles devoted to pallidotomy, and, accordingly, the results of treatment of 1510 patients, the following complications of this operation were identified: The effectiveness of pallidotomy in Parkinson’s disease is quite high. Hypokinesia in the limbs opposite to the operation is reduced in 82% of cases.

With the development of radiosurgery, a new opportunity has appeared to destroy the corresponding nerve structures without traumatizing the surrounding structures and tissues.

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Doctor73 – News – Head of the neurological department of the UOKB Tatyana Fedotova: “Timely diagnosis is very important to preserve the quality of life of patients with Parkinson’s disease”

April 11 – World Parkinson’s Day is celebrated annually at the initiative of the World Health Organization.After Alzheimer’s disease, this disease is the most common neurodegenerative disease affecting older people. Tatyana Vasilievna Fedotova, head of the neurological department of the Ulyanovsk Regional Clinical Hospital, told us about what kind of movement disorders are characteristic of this disease.

– Tatyana Vasilievna, what is this disease and how often does it occur?

– Parkinson’s disease is a chronic neurological disease associated with the death of motor nerve cells that produce dopamine.This substance induces feelings of pleasure and is used by the brain for evaluation and motivation. If dopamine is not produced in sufficient quantities, a person becomes inert, the cognitive process slows down, a limited number of thoughts and ideas dominate in consciousness. The prevalence of Parkinson’s disease is 85-187 cases per 100 thousand population. The average age of onset is 55-58 years. At the same time, about 10% of patients experience the so-called earlier onset – up to 40 years. It often takes 2-3 years from the onset of the first symptoms to the diagnosis.Timely diagnosis is essential for correct treatment and preservation of the patient’s quality of life. Outward signs of Parkinson’s disease are tremors (tremors) – initially it manifests itself in the multidirectional movement of the fingers of one hand, then it spreads to the other hand, manifests itself in shaking the head, trembling of the eyelids, tongue, and lower jaw. In a person suffering from Parkinson’s disease, the tremor occurs at rest, with excitement, it intensifies, during sleep it subsides. There are cases when the tremor covers the entire body of the patient.There may also be spontaneous physical activity, stiffness of movements, “puppet gait”, when the patient, when walking, puts his feet parallel to each other and holds his hands motionless, a frozen expression on his face, a stopped gaze. A person with Parkinson’s disease can spend hours in the same position. Monotonous speech devoid of expressiveness, small handwriting with “torn” lines. The patient cannot simultaneously perform several purposeful movements. Muscle rigidity is manifested in an increase in muscle tone; when flexing or extending the limbs, they freeze for a while in one position.The “supplicant’s pose” characteristic of Parkinson’s disease is formed: the patient stands hunched over, tilting his head forward and bending his knees, half-bent hands tightly pressed to the body. Difficulty in overcoming both rest inertia and movement inertia manifests itself in the later stages of the development of the disease. It is difficult for the patient to start moving, and once moving, it is difficult to stop. Vegetative and mental disorders lead to metabolic disorders, can cause exhaustion or, conversely, obesity.Secretory disorders are expressed in the active secretion of sebum, excessive salivation, sweating. In a patient with Parkinson’s disease, depending on the clinical form of the disease, not all possible movement disorders may appear, but only some of them. Slowness of movement when walking, dressing, eating, writing disorder, problems when brushing teeth, shaving are the first symptoms of the disease. Jumping movement, when walking is abruptly replaced by running, salivation due to the inability to perform swallowing movements also indicate the possible development of Parkinson’s disease.

-Which specialists should you contact if you notice characteristic symptoms of the disease in yourself or your loved ones?

– It is necessary to consult a neurologist, undergo electromyography and electroencephalography. At the first signs of Parkinson’s disease, it is recommended to adhere to a low-cholesterol and low-protein diet, and engage in physiotherapy exercises. Flavonoids contained in tea (especially green), cocoa, fresh fruits (apples, peaches, apricots, quince, oranges), berries (raspberries, currants, strawberries) help reduce the risk of disease.

For information:

Parkinson’s disease was first described by James Parkinson in his Essay on Shaking Palsy in 1817. Parkinson’s disease was officially recognized by the Vatican in 2003, but Pope John Paul II has suffered from this disease since 1993. She impressed Mao Zedong in the last years of his life. Erich Honnecker, who led the German Democratic Republic for many years, also fell victim to Parkinson’s disease. Spanish dictator Francisco Franco stepped down as prime minister after being similarly diagnosed.Parkinson’s disease caused the death of the poet Andrei Voznesensky. Salvador Dali, mathematician Andrei Kolmogorov and British writer Arthur Koestler suffered from this ailment.