| ID | 120 |
|---|---|
| Name | PARKINSONISM |
| Cause | |
| Signs Symptoms | |
| Diagnosis | |
| Investigations | Investigations: Usually diagnosis is made on clinical grounds; detailed investigations don’t require. Some exceptions may be required to exclude as following- 1. Serological tests for syphilis 2. CT scan of brain 3. Test to exclude Wilson’s disease |
| Management | Management: Drugs used in parkinsonism: 1. Levodopa- it is an amino acid precursor of dopamine, acts mainly by replenishing depleted striatal dopamine; it improves bradykinesia and rigidity more than tremor. It is generally administered in conjuction with an extracerebral dopa-decarboxylase inhibitor e.g carbidopa or benserazide, to prevent peripheral conversion of levodopa to dopamine, so maximum levodopa enters in the brain by crossing blood brain barrier, but decarboxylase inhibitors can’t cross blood brain barrier; as a result patients save from high incidence of side-effects of excess dopamine in the peripheral circulation. Dose: Levodopa 50mg 8-12 hourly increasing gradually over 2-4 weeks to 100mg 8 hourly; may be increased up to 1000mg/day, but should be kept as low as possible. Combined preparation: Co-careldopa, a combined preparation of carbidopa & levodopa is available in different usual proportions, such as-i. 10mg of carbidopa for each 100mg of levodopa ii. 25mg of carbidopa for each 100mg of levodopa iii. 25mg of carbidopa for each 250mg of levodopa. 2. Anticholinergic drugs (e.g benzhexol, or orphenadrine)- these are effective in the treatment of tremor and rigidity, but not bradykinesia, so they are usually advised in the early stage parkinsonism. Dose: benzhexol l-4mg-8 hourly; orphena-drine 50-100mg 8 hourly. 3. Amantadine- it is originally introduced as an antiviral agent, but also found helpful in parkinsonism; it has a short-lived mild effect oh bradykinesia, so may be used in the early stage, while bradykinesia in not prominent. Dose: 100mg 8 or 12 hourly. 4. Bromocryptine- it is a dopaminergic agonist, directly acts on dopaminergic receptors mainly Dl & D2, & also on D3- 5. It is used in parkinsonism as an alternative or an addition to levodopa. Dose: initially. l-2.5mg daily with food then dose will be increased slowly to 2.5mg 8 hourly over 1st week & thereafter increased up to 30mg daily. Therapeutic strategy: Early stage: Under age 65- Anticholinergics Amantadine, Over age 65- Amantadine, Avoid anticholinergics Moderate stage: Levodopa combinations (e.g levodopa + carbidopa, known as co-careldopa or levodopa + benserazide, knwon as beneldopa) Anticholinergics In young petient- low dose bromocriptine + levodopa combination may be given Severe stage: Frequent small doses of levodopa combination (1.5-3 hourly) ± Low dose bromocryptine 15-30mg/day |
| Introduction | James Parkinson described ‘Parkinsonism’ as the syndrome comprising three main components- tremor, muscular rigidity & hypokinesis (or bradykinesia). Hypokinesis or bradykinesia describes slowness in initiating and repeating voluntary movements, despite normal muscular strength (akinetic-rigid syndromes). Parkinson’s diasese: ‘Parkinsomism’ of idiopathic origine, known as Parkinson’s disease or idiopathic Parkinson’s disease, is the most common type of movement disorders belonging to akinetic-rigid syndromes. |
| History | |
| Etiology | |
| Clinical Features | Clinical features: Symptoms: Patients usually complain of- 1. Slowness of movement with tremor & rigidity in the limbs, as a result, difficulty in rising from sitting or getting into or out of bed. 2. Impairment of fine movements of limbs, causing hand writings smaller & spidery, which usually tail off and end at a line. Physical signs: General signs-Appearance is expressionless Skin appears to be greasy Patient usually stands with flexed posture. Gait & movement- Slowness in starting walking or movement Small, but rapid steps Reduced arm swinging Difficulty in turning movement , Poor precision of repetitive movements. Tremor-Tremor at rest- frequency 4-7 Hz, usually first in fingers or thumb, diminishes on action & increase by emotion; may affect one or both hands. Pill-rolling movements between the thumb & forefinger may be present. Tremor at posture- frequency 8-10 Hz, less.distinct but faster with finer amplitude; present on action & also persists with movement. Rigidity-Rigidity of the upper limbs, which is cogwheel type hi most cases. Lead pipe type rigidity, mostly eppers in thejegs. Stiffmess of trunk, usually presents as flexed stooped posture. |
| Preventions | |
| Treatment | |
| Complications | |
| Prognosis | |
| Types | Clinical stages of Parkinson’s disease: 1. Early stage- when there is only tremor & rigidity. 2. Moderate stage- tremor, rigidity & bradykinesia. 3. Severe stage- tremor, rigidity, bradykinesia & dyskinesia with fluctuations. |
| Classification | |
| Observation | |
| Pathology | Pathology: Basic pathology of parkinsonism is depletion of dopaminergic neurones in the substantia nigra & locus coeruleus of brain. As a result, dopamine output from the substantia nigra becomes very low, as a consequence the inhibitory effects on the subthalamic nucleus is reduced & as a result the neurones of which become more active than usual in inhibiting functions of the cerebral cortex, resulting in bradykinesia |
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