Movement Disorder
Movement Disorder
Movement Disorder
oscilations around a fixed point occur at rest outstretching (postural), during anxiety, caffeine drugs On action (intention) :
Cerebral
Essential
tremor : retlatively benign, embarrasing disorder, familial, sporadic forms, aggravated by stress,excitement tremor : involuntary torsion movement, affected muscle group, movement ussually slow
tremor (Parkinsonism)
Dystonic
Resting
Exaggerated
Upper
action
Bilateral, Tremor No
Primodone
Propanolol
blockers
Tremors
of some patients are quite responsive to alcohol, and patients may selfmedicate
A. HYPERKINESIA
Tremor
Excessive spontaneous movements , rapid, arrhytmic movements of muscle group The movement are often incorporated into deliberate movements by the patient to camouflage their disorder Irreguler, brief and aburpt non stereotype (non repetitive) Distal predominance Facial grimacing
Medications
Huntingtons
disease
Hemibalism
Post-infection
1. Chorea sydenham 2. Huntington disease 1. Chorea sydenham Acute movement Paroxismal Uncoordinated movement Involuntary Emotional disturbances Diminish while sleeping and increase by stress
Clinical appearance Choreatic Cognitive dysfunction Gait disorder Clumsiness Speech disorder Bladder and bowel incontinence Sexual dysfunction
Valproic
Carbamazepine Corticosteroid
Dopaminergic
Dystonia is a slow, purpose, involuntary movements affecting muscle groups of face, limb, trunk Agonist and antagonist Clinical findings :
movement charactherized by slow, writhing of groups of muscle More pronounce in the distal extremities Associated with weakness and rigidity Aggravated by stress Disappears during sleep Athetosis is slower than chorea and may occur together
Definition
: brief, sudden, irresistible, inapposite, reccurent movement These movements are either isolated or represent an act for a particular purpose For a time tics can be suppresed or inhibited Patients often feel actively in performing a tic Tics can be tiggered by environmental stimuli, exciting events or life event
B. HYPOKINESIA
Spasticity Drop attack
Parkinsons
disease is a chronic neurodegenerative disease associated with substantial morbidity, increased mortality, and high economic burden results from the degeneration of dopamine-producing nerve cells in the brain, specifically in the substantia nigra.
Parkinsons
The most common movement disorder affecting 1 2 % of the general population over the age of 65 years. Prevalence rate in men are slightly higher than in women Age onset usually between 50-70 years Rarely in people less than 30 years old Incidence is 20 every 100.000 population
Age - the most important risk factor Positive family history Male gender Environmental exposure: Herbicide and pesticide exposure, metals (manganese, iron), well water, farming, rural residence, wood pulp mills; and steel alloy industries Race Life experiences (trauma, emotional stress, personality traits such as shyness and depressiveness)? An inverse correlation between cigarette smoking and caffeine intake in case-control studies
Its widely believed that genetic and enviromental factor induce neuronal death
The most common pathological feature is degeneration of dopaminergic neurons in pars compacta of substansia nigra The lost of dopaminergic neuron decreased activity of thalamus,thus reducing excitatory input to motor cortex and initiate ivoluntary movement The presence of lewy bodies is another classic pathological finding in parkinson disease
Four
cardinal symptoms:
Resting tremor Bradykinesia (generalized slowness of movements) Muscle rigidity Postural instability
Resting tremor: most common first symptom, usually asymmetric and most evident in one hand with the arm at rest. Shaking or trembling in the hand, arm, leg, face, and it spreads, sometimes affecting only one side of the body.
Worsen when the muscles are relaxed or individual is stressed Dissapears during sleep or during intentionally moved
Bradykinesia: spontaneus and automatic movement are lost and all movement becomes extremely slow. Diffiulty with daily activities such as writing, shaving, using a knife and fork and opening buttons Decreased blinking, masked facies, slowed chewing and swallowing.
Rigidity: muscle tone increased in both flexor and extensor muscles providing a constant resistance to passive movements of the joints Stooped posture, anteroflexed head, and flexed knees and elbows.
Postural instability: due to loss of postural reflexes. balance and coordination become impaired. Patients tend to lean forward or backward, and to develop a stooped posture. Walking with quick and small steps.
Dysfunction of the autonomic nervous system: impaired gastrointestinal motility, bladder dysfunction, excessive head and neck sweating, and orthostatic hypotension. Depression: mild to moderate depression in 50% of patients.
Cognitive impairment: mild cognitive decline including impaired visual-spatial perception and attention Slowness in execution of motor tasks At least 1/3 become demented during the course of the disease.
Difficulty swallowing or chewing Urinary problems Constipation Irregular sleep Short breathing
Include :
mental
health problems depression psychotic symptoms dementia sleep disturbance falls autonomic disturbance
No
Diagnosis Depends
on the presence of at least two of the three major signs : tremor at rest, rigidity, and bradykinesia. is tested by determining how quickly the person can tap the finger and thumb together.
Bradykinesia
Possible
Alt least one of TRAP symptoms (tremor, rigiditas, akinesia, postur tak stabil)
Probable
Definite
Combining 3 of 4 major symptoms or 2 symptoms with another asymetrical symptom (3 cardinal signs)
The goal of therapy is to reverse functional disability, abolition of all symtoms and signs is not currently possible even with high dose of medication Treatment highly individualized no universal first choice drug therapy choice of adjuvant drug should take into account clinical and lifestyle characteristics patient preference
1.
Supporting treatment
2.
Medication
NMDA antagonist : amantadine (symetrel) 100-300mg/day Dopaminergic : carbidopa+levodopa 10/100mg, 25/100mg, 25/250 mg Dopamine agonist : bromocryptine 5-40mg/day pramipexole 1,5-4,5 mg/day
ropinirole 0,75-2,4mg/day
2.
Operative treatment
2.
psychotherapy
make
PD
monitoring and alteration of medication a continuing point of contact a reliable source of information
1.
Waters CH. Diagnosis and maanagement of Parkinsons disease, second edition. Caddo, Professional Communications nc; 1999: 31-71. Basjiruddin A. Management of lates Parkinsons disease. In: Sjahrir H, dkk (eds). Parkinsons disease and other movement disordres. Medan; 2007: 124-43. Wolters EC, Bosboom JLW. Parkinsons disease. In: Wolters et al (eds). Parkinsonism and related disorders. Amsterdam, VU University Press; 2007:143-155. Parkinsons: Clinical features and differential diagnosis. Fahn S, Jankovic J. Principles and practice of movement disorders. Philadelphia, Churchill Livingstone Elsevier; 2007: 79-96. Benazzouz A. Parkinsons disease and implication of basal ganglia in its pathoophysiology. Egypt, June 2009. NHS National Institu for Health and Clinical Excellence. Parkinsons disease.June, 2006
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