Деякі причини вторинного та атипового паркінсонізму
Cause | Comments |
|---|---|
Neurodegenerative disorders | |
Amyotrophic lateral sclerosis–parkinsonism-dementia complex of Guam | Responds poorly to antiparkinsonian medications |
Corticobasal ganglionic degeneration | Begins asymmetrically, usually after age 60 Causes cortical and basal ganglia signs, often with apraxia, dystonia, myoclonus, and alien limb syndrome (movement of a limb that seems independent of the patient’s conscious control) Causes immobility after about 5 years and death after about 7–10 years depending on the cause Responds poorly to antiparkinsonian medications |
Dementia (eg, Alzheimer disease, chromosome 17–linked frontotemporal dementias, diffuse dementia with Lewy bodies) | Parkinsonism often preceded by dementia most typically with
|
May include prominent autonomic dysfunction (orthostatic light-headedness, urinary or fecal incontinence) May include prominent cerebellar dysfunction May include severe parkinsonian features, usually with poor response to levodopa May include pyramidal signs Often causes early falls and balance problems Responds poorly to antiparkinsonian medications | |
First manifests with gait and balance problems In its classic form, causes progressive ophthalmoparesis, starting with impairment of downward gaze Responds poorly to antiparkinsonian medications | |
Spinocerebellar ataxias (usually type 1, 2, or 3) | Usually first manifests with imbalance and poor coordination but may have additional classical symptoms (eg, pyramidal tract signs in type 1, slow saccades and polyneuropathy in type 2, parkinsonism and dystonia in type 3) Responds poorly to antiparkinsonian medications |
Other disorders | |
Cerebrovascular disease | Manifests with rigidity and bradykinesia or akinesia (akinetic-rigid syndrome) that predominantly involves the lower extremities, with prominent gait disturbance and symmetric symptoms Rarely responds to antiparkinsonian medications and, if it responds, may require high levodopa doses (at least 1000 mg a day) |
Brain tumors near the basal ganglia | Manifests with hemiparkinsonism (ie, restricted to the side of the body opposite the lesion) |
Chronic traumatic encephalopathy (due to repeated traumatic brain injury) | Characterized by progressive parkinsonism, dementia, and mood disorders, including suicidal ideation Formerly known as dementia identified in boxers but now recognized in participants in various contact sports and in soldiers with blast injuries |
Usually characterized by normal CSF pressure and caused by various mechanisms (eg, increased CSF pulsatility, reduced CSF drainage [1]) | |
Causes calcification of the basal ganglia May cause parkinsonism, chorea, and athetosis | |
Viral encephalitis (eg, West Nile encephalitis), infectious or postinfectious autoimmune | Can cause parkinsonism transiently during the acute phase or, rarely, permanently (eg, postencephalitic parkinsonism after the epidemic of encephalitis lethargica in 1915–1926) In postencephalitic parkinsonism, forced, sustained deviation of the head and eyes (oculogyric crises); other dystonias; autonomic instability; depression; and personality changes |
Medications | |
Can cause reversible† parkinsonism (drug-induced or pharmacologic parkinsonism) | |
Meperidine analog (N-MPTP)‡ | Can cause sudden, irreversible parkinsonism due to a contaminant in the illicit preparation of meperidine Occurs in people who use IV drugs |
Metoclopramide Prochlorperazine Reserpine (not available in the United States) Lithium, long-term use | Can cause reversible† parkinsonism May be dose-dependent or related to susceptibility (risk factors include older age and female sex) With lithium, sometimes results in cerebellar dysfunction; may occur in patients with serotonergic syndrome |
Toxins | |
Carbon monoxide | Can cause irreversible parkinsonism due to bilateral internal globus pallidus necrosis |
Methanol | As contaminated moonshine, can cause hemorrhagic necrosis of the basal ganglia |
Manganese | Can cause parkinsonism with dystonia and cognitive changes when toxicity is chronic; cock walk gait§ is characteristic, as well as T1-weighted hyperintensity in the lenticular nucleus Usually related to occupation (eg, in miners or industrial workers) but can result from abuse of methcathinone (a metabolite of ephedrine), which causes a form of presumed manganese poisoning that has been reported in people who use IV drugs and inject self-prepared methcathinone |
* Language impairment may involve expressive (nonfluent primary progressive) aphasia or receptive (primary progressive semantic) aphasia. | |
† When medications are withdrawn, symptoms usually resolve within a few weeks, although they may persist for months. | |
‡ N-MPTP results from unsuccessful attempts to produce meperidine for illicit use. | |
§ Features of dystonic gait include toe-walking, flexed elbows, and an erect spine. | |
CSF = cerebrospinal fluid; N-MPTP = N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. | |