Extrapyramidal syndrome Presented by Ri

DefinitionNeurologic syndromes in which abnormal movement occur due to a disturbance of fluency and speed of voluntary movement or the presence of unintended extra movements

Pathogenesis1Results from dysfunction of the extrapyramidal systemBasal ganglioncaudate, putamen, globus pallidus, subthalamic nucleus, and substantia nigra motor area of cortex--> basal gangalion(organizing movement commands) --> motor area of cortex affects the size and speed of movementsselection of components of movements or the sequencing of multi-step movements

Pathogenesis2Direct pathwayDopamine D1 type medium spiny neuron internal portion of globus pallidus ventral anterior/ventral lateral region of thalamus cortexIndirect pathwayDopamine D2 type medium spiny neuron external portion of globus pallidus subthalamic nucleus internal portion of globus pallidus ventral anterior/ventral lateral region of thalamus cortex

Pathogenesis3

Drug-induced EPS(1)EPS secondary to pharmacologic agents are the most common.The risk of developing a drug-induced EPS begins at the onset of treatment with an offending agent.Acutely: within hours or a few daysSubacutely: over several weeksLate or delayed onset: six months or longer after exposure(tardive) short-term therapy of minimal therapeutic dosages should be the strategy employed

Drug-induced EPS (2)Five classes of drugs are known to affect central dopaminergic systemsCentral stimulantsact as indirect dopamine agonist ex. AmphetamineLevodopaa precursor of dopamineDirect dopamine agonistex. BromocriptinePresynaptic dopamine antagonists ex. ReserpineAntagonize or block central dopamine receptors neuroleptics, metoclopramideprimperam

ManifestationAcute dystoniaParkinsonismAkathisiaTardive dyskinesia

Acute dystonia Definition long-lasting contraction or spasm of musculaturegenerally less common than most other extrapyramidal symptomsyoung age and male sex predominantThe pathophysiological mechanism is presently unknown Diagnosis: The most common muscle groups affected are the eyes, jaw, tongue, and neck trismus, blepharospasm, oculogyric crisis, torticollis, opisthotonus, laryngeal spasmmost dangerousTreatment anticholinergic drug. Ex. Benztropine, diphenhydramine

ParkinsonismPathophysiology: blockade of postsynaptic dopamine(D2) receptors in the corpus striatumDiagnosisthree cardinal symptomsTremor(1)steady, rhythmical, oscillatory motion(2)the most affected body area tends to be the upper extremities(3)typically suppressed during action and increase during times of anxiety, stress, or fatigue Muscle rigidity(1)firmness and spasm of muscle at rest(2)generalized muscle pain, body aches, and discoordination are associated features

ParkinsonismAkinesia(1)decreased spontaneous motor activity and a global slowness in the initiation and execution of movements(2)associated with drooling, bent over neck, stooped shoulders, and masked facial expressionTreatmentLower dose of agentSwitching to a low potency agentAnticholinergic drugs

AkathisiaDefinition a sense of motor restlessness in which the patient feels a constant need to move about.The most common type of EPSPathophysiology: unknownDiagnosis tend to have subjective complaints of inner restlessness most often in legsThey feel that they must move, and this manifests as frequent changes in posture, crossing and uncrossing of the legs.. Often associated with severe dysphoria, anxiety, and irritability

AkathisiaTreatmentLower dose of agentSwitching to a low potency agentAnticholinergic drugsbeta-adrenergic blockersbenzodiazepine

Tardive dyskinesiaDefinition a syndrome of abnormal movements following at least six months and often many years of drug therapyPathophysiology denervation-hypersensitivity phenomenonIt appears with prolonged receptor blockade, the receptors rebound, becoming supersensitizedDiagnosisCharacterized by involuntary movement of the lips, tongue, jaw, and extremities

Tardive dyskinesiaLipsmacking, facial and lingual masticatory movements, trunk rocking and restless foot movementsReduced by voluntary movements of the affected areasIncreased by voluntary movements of unaffected areasIncreased with emotional arousalAbsent when the individual is asleepTreatmentThe best treatment is preventiongradual reductionLow dose of benzodiazepineDopamine antagonistDopamine depleting agents

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