Neuroscience (Movement Disorders) Flashcards
State the 3 importance of basal ganglia
- regulation of movement quantity
- learning
- emotion
State the 6 causes of parkinsonism
- idiopathic parkinson disease
- parkinson plus syndrome
- neuroleptic medication
- wilson disease
- infective encephalitis
- vascular parkinsonism
State the 2 characteristics of idopathic parkinson disease
- asymmetric parkinsonism
- apoptosis of nigro-striatal neurons due to accumulation of alpha-synuclein in lewy bodies with dopaminergic neurons due to alpha-synuclein gene
State the clinical triad of motor symptoms for parkinsonism
- lead pipe rigidity
- bradykinesia
- resting tremor
Explain the difference between the rigidity in
(1) UMN lesion
(2) Parkinsonism
(1) UMN lesion = knife-clasp rigidity - resistance varies depending on position of joint
- due to certain sets of muscles being much stronger than their antagonists –> tone in joint predominantly determined by stronger muscle
(2) Parkinsonism = lead pipe rigidity - resistance remains unchanged regardless of position of joint
- due to both agonistic and antagonistic muscles being as rigid as each other –> joint is held tight and rigid by opposing muscles regrdless of position
Expand on the clinical presentations of bradykinesia affecting patients with parkinsonism.
- poverty of movements
- hypomimia
- paucity of blinking
- hypophonia
- micrographia
- decremental bradykinesia
- festinant gait
- smaller stride
- reduced arm swing walking
Recap the 3 times of tremors in neurologic conditions.
Name a condition associated with each tremor
- resting tremor - parkinsonism
- intention tremor - cerebellar pathologies
- postural tremor - benign essential pathologies
State the non-motor symptoms of parkinsonism
- mood - depression, hallucinations, psychosis
- sleep - sleep disturbances, sleep fatigue, disorders (REM sleep disorder, excessive daytime sleepiness, insomnia)
- cognitive - dementia, cognitive deficits
- autonomic - incontinence, incompetence, postural hypotension, sialorrhoea, anosmia, constipation
State the gold standard of treatment for parkinsonism.
State the reason why dopamine should not be administered.
State the reason why a precursor is given on top of medication.
GOLD STANDARD OF TREATMENT = L-DOPA + CARBIDOPA
- madopar, sinemet
(1) WHY SHOULD DOPA NOT BE ADMINISTED
- dopamine too large to cross BBB –> will be deposited in gut instead of target organ (brain) –> inefficient
- Dopamine is a positive ionotrope –> causes tachycardia
(2) WHY SHOULD A PRECURSOR BE GIVEN
- Carbidopa inhibtis dopa carboxylase which converts L-DOPA to dopamine
- Without carbidopa, L-dopa converted to dopamine which is too large to cross BBB –> will still be deposited at sites other than target organ
State everything you know about Wilson’s disease
WILSON’S DISEASE
- One of the causes of Parkinsonism
- Defect in biliary copper excretion –> excess copper deposited in liver, basal ganglia and eyes
- AR inherited metabolic disorder
- treatment = sequester copper by penicillamine
Diagnosis:
- demonstrate low levels of ceruloplasmin (copper transporter)
- demonstrate high copper urine levels
- demonstrate kayser flesicher rings in eyes
- in the presence of parkinsonism or liver issues (cirrhosis)
State the involvement of each pathway in physiologic repsonse:
1. Nigro-striatal pathway
2. Meso-cortical pathway
3. Locus coerulus
4. Dorsal raphe nuclei
- Nigro-striatal pathway = involved in movement (parkinsonsim)
- Meso-cortical pathway = involved in mood, motivation and reward (depression)
- Locus coerulus = involved in mood
- Dorsal raphe nuclei = involved in mood and sleep
State the 3 pathways that dopamine is involved in. State the corresponding conditions linked to each pathway
Nigrostriatal pathway - too little dopamine - parkinsonism
Mesocortical & Mesolimbic pathway - too much dopamine - schizophrenia
Tuberoinfundibular pathway - too little dopamine - hyperprolactinaemia
