Dr. Kolapo K. O Department of Internal Medicine, U.B. SOM.

The motor system consists of; The Pyramidal, Extrapyramidal system and cerebellum. The pyramidal system consists of; Corticospinal tract Extrapyramidal system consists of; Basal ganglia Sustantia nigra. Subthalamic nucleus Red nucleus.

Pyramidal tract lesion leads to; Hemi/quadric/paraparesis depending on the level and site of lesion. Deep tendon hyperreflexia Hypertonia +ve Babinski sign Absent abdominal reflex Hemiplegic (Unilateral pyramidal lesion)/scissors gait (bilateral pyramidal lesion).

Exrapyramidal tract lesion can be; Hypo/hyperkinetic movement disorders. Hypokinetic movement dosrders;.

.

Parkinsons disease is the prototype hypokinetic disorder caused by degeneration/loss of dopaminergic neurons in the substantia nigra, leading to depletion of dopaminergic transmission and abnormal activitiy in the basal ganglia as a whole. This lead to;A

increase in the activity of the indirect GABA ergic pathway. An increase in the activity of the cholinergic transmission.

PDParkinsons Disease

Muhammad Ali in Alanta Olympic

normal

Together, the loss of substantia nigra dopaminergic neurons and the presence of Lewy body inclusions are regarded as the hallmark of idiopathic Parkinsons disease pathology.

Most

symptoms do not appear until the striatal dopamine level declines by at least 70-80%. Onset typically between 50-60 years of age, and slowly progresses with age

Idiopathic

Parkinsons disease is the most common variant of parkinsonism, accounting for over 80% of all parkinson syndromes seen in the general population

Cerebral

atherosclerosis Viral encephalitis Side effects of several antipsychotic drugs (phenothiazines, reserpine,butyrophenones).

Rare

causes of parkinson syndrome are MPTPinduced parkinsonism, carbon monoxide poisoning,.

Features include; Akinesia and bradykinesia (Slowness

of Movement-

Difficulty in Initiation and Cessation of Movement) Rigidity. Resting tremors (pill rolling). Postural instability. Mask-like facie.

Monotonous

speech. Reduced arm swinging. Micrographia. Shuffling or festinant gait. Propulsion and retropulsion (difficulty in voluntarily stopping when pushed forward or backward)

diminished

sense of smell

low voice volume foot cramps sleep disturbance depression constipation drooling

Dopaminergic agents Levodopa/carbidopa Dopamine agonists; Bromocriptine, Cabergoline,

Lisuride, Pergolide, Pramipexole, Ropinirole. COMT inhibitors; tolcapone, entacapone MAO-B inhibitors:Seleginine Anticholinergics:Trihexyphenidyl: 2-15 mg/day Benztropine: 1-8 mg/day

Amantadine:

enhancing release of stored dopamine inhibiting presynaptic reuptake of catecholamines dopamine receptor agonism NMDA receptor blockade

Substantia NigraAmantadine* levodopa

selegiline

Dopamine agonists bromocriptine pergolide pramipexole ropinirole

DA

GABA

BBB carbidopa benserazide tolcapone entacapone

ACh

baclofen trihexiphenidyl

Striatum

caudate nucleus is the site of the lesion Involuntary, irregular, jerky movement; affect head, neck face and shoulders commonly. Described as dance-like movement. Patient has semi-purposive movement. Athetosis (putamen is the site of lesion). Chorea is often accompanied by athetosis in which the abnormal movements are slower, more writhing (snake-like) affecting the hands and fingers and worsened by physical activities and emotion.

Choroathetosis often occur together are usually abolished by sleep.

Benign hereditary, senile. Huntingtons disease. Wilsons disease. Syndehans chorea, chorea gravidarum, SLE, hyperthyroidism. Drugs (tardive chorea); Ldopa, OCP, amphetamine,cocaine abuse.

Dystonia Sustained torsion spasms of muscle contraction which distort the limbs, trunks or face into characteristic postures.

Focal, segmental, hemidystonia, generalized dystonia. Abnormal movements are not present during sleep and areenhanced by emotional stress or voluntary activity. Etiology

Perinatal hypoxia, birth trauma, kernicterus.Hemibalismus (site of lesion is subthalamus). Unilateral large amplitude flinging of the limbs, especially in proximal limb muscles.

- Usually results from CVA (Cerebrovascular Accident) involving subthalamic nucleus - sudden onset - Violent, writhing, involuntary movements of wide excursion confined to one half of the body - The movements are continuous and often exhausting but cease during sleep - Sometimes fatal due to exhaustion - Could be controlled by phenothiazines and stereotaxic surgery

Lesion: Subthalamic Nucleus

Etiology

Ischemic or hemorrhagic vascular lesions. Diffuse encephalitis, SLE, AIDS, head injury, tumors, A-Vmalformations. Due to lesion in the contralateral subthalamic nucleus.

Myoclonus Rapid shock-like muscle jerks which are often repetitive and sometimes rhythmic. GENERALISED; widespread distribution. Physiologic; occurring during falling asleep or awakening (nocturnal myoclonus); and hiccups. Essential; benign condition, sometimes inherited, occurring in absence of other neurologic symptoms. Epileptic; seizure disorder predominates. Symptomatic; part of another disorder hepatic/renal, degenerative (wilsons, alzheimers,Huntington;s), infectious (SSPE, AIDS). SEGMENTAL; restricted to a particular part of the body. arise from lesion affecting the CNS.

Tics Brief, rapid, involuntary movements, often resembling fragments of normal behaviour.

most frequent forms ;blinking, sniffing, throat clearing. Simple(eye blinking). complex.

Clinical features Tremor on intention. Speechdysarthria. Ataxic gait, dysdiadocokinesia, truncal ataxia. Hypotonia, Pendular reflexes. Nystagmus, Rebound phenomenon, vertigo. Dysmetria (pre & past-pointing). Motor ataxic gait if bilateral. Reeling gait in unilateral lesion.