APPROACH TO THE PATIENT Movement Disorders
Divided into akinetic rigid forms, with muscle rigidity and slowness of movement, and hyperkinetic forms, with involuntary movements. In both types, preservation of strength is the rule. Most movement disorders arise from disruption of basal ganglia circuits; common causes are degenerative diseases (hereditary and idiopathic), drug induced, organ system failure, CNS infection, and ischemia. Clinical features of the various movement disorders are summarized below.
Inability to initiate changes in activity or perform ordinary volitional movements rapidly and easily. There is a slowness of movement and a paucity of automatic motions such as eye blinking and arm swinging while walking. Usually due to Parkinson’s disease or other causes of parkinsonism (Chap. 186).
Rhythmic oscillation of a part of the body due to intermittent muscle contractions, usually involving the distal limbs and less commonly the head, tongue, or jaw. A coarse tremor at rest, 4–5 beats/s, is usually due to Parkinson’s disease. A fine postural tremor of 8–10 beats/s may be an exaggeration of normal physiologic tremor or indicate familial essential tremor (ET). An intention tremor, most pronounced during voluntary movement toward a target, is found with cerebellar pathway disease.
This is the most common movement disorder, affecting approximately 5% of the population. It can present in childhood but dramatically increases in prevalence over the age of 70 years. The tremor is most often manifest as a postural or action tremor and, in severe cases, can interfere with functions such as eating and drinking. It is typically bilateral and symmetric but may begin on one side and remain asymmetric. Tremor involves the head in ∼30% of cases, voice in ∼20%, tongue in ∼20%, face/jaw in ∼10%, and lower limbs in ∼10%. Multiple body parts are involved in at least 50%. The tremor is characteristically improved by alcohol and worsened by stress. The tremor of ET must be distinguished from dystonic tremor and early Parkinson’s disease (Table 56-1). The pathophysiology of ET is unknown. Approximately 50% of cases have a positive family history with autosomal dominant inheritance.
TABLE 56-1Advanced Examination Pearls: Differentiating Essential Tremor from Parkinsonian Tremor |Favorite Table|Download (.pdf) TABLE 56-1Advanced Examination Pearls: Differentiating Essential Tremor from Parkinsonian Tremor
| ||ESSENTIAL TREMOR ||PARKINSONIAN TREMOR |
|Speed ||5–10 Hz ||4–6 Hz |
|Symmetry ||Bilateral ||Usually asymmetric |
|Most common component ||Postural ||Rest |
|Other parkinsonian symptoms ||Absent ||Present |
|Helped with alcohol ||Usually ||Rarely |
|Family history ||Present often ||Usually absent |
Many pts with ET have mild symptoms and require no treatment.
When activities of daily living such as eating and writing are impaired, therapy with propranolol (20–120 mg/d) or primidone (12.5–250 mg tid) benefits ∼50% of pts; hand tremor tends to be most improved, while head ...