neuro Flashcards
wtf is parkinson’s disease?
progressive reduction of neurotransmitter dopamine which is produced by substantia nigra in basal ganglia (deep in cerebral hemispheres, structures containing nerve cell bodies for habitual motor control eg. walking, looking around) = leads to disorders of these movements (asymmetrical - one side affected more than other)
classic triad of parkinson’s disease features?
resting tremor = 4-6 Hz/times per second “pill rolling tremor” - more pronounced when resting, improves on voluntary movement, worse when distracted eg. asked to use other hand for smth else
rigidity = resistance to passive movement of joint “cogwheel rigidity” - if flex/extending patient’s arm at elbow you will feel tension leading to little jerks (cogwheel)
bradykinesia = smaller/slower movements eg. small handwriting, shuffling gait, difficulty initiating movement (standing still to walking), difficulty turning around, reduced facial movements (hypomimia/masking)
typical presentation of parkinson’s disease?
older man (70 yrs) stooped posture facial masking (facial muscles expressing emotion - rigid/slow to respond) forward tilt reduced arm swing shuffling gait
other features affecting parkinson’s patients?
depression, sleep disturbance/insomnia, loss of sense of smell (anosmia), postural instability, cognitive impairment/memory problems
parkinson’s tremor vs benign essential tremor
P = asymmetrical, 4-6Hz, worse at rest, improves with intentional movement, other features, no change with alcohol BE = symmetrical, 5-8 Hz, improves at rest, worse with intentional movement, no other parkinson’s features, improves with alcohol
wtf is dementia with Lewy bodies ?
type of dementia associated with parkinsonism - causes a progressive cognitive decline
on a spectrum: if dementia is presenting issue = DLB, if parkinson’s is issue = parkinson’s dementia
eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in brainstem and neocortex
substantia nigra depigmentation and amyloid deposits
wtf is multiple system atrophy ?
rare parkinson’s related condition, neurones of multiple systems in brain degenerate. affects the basal ganglia (parkinson’s presentation). other areas affected lead to autonomic dysfunction (sexual dysfunction, abnormal sweating, constipation, hypotension) and cerebellum dysfunction (ataxia - coordination, balance, speech affected)
managing parkinson’s: synthetic dopamine?
no cure, treatment focussed on controlling/minimising symptoms
Levodopa (synthetic dopamine) with peripheral decarboxylase inhibitors (carbidopa, benserazide) which stop levodopa being broken down in body before it gets to brain. combo drugs = co-benlydopa, co-careldopa
this is less effective over time, side effect of dopamine is dyskinesias (excessive motor activity leads to abnormal movements) eg. dystonia (excessive muscle contraction creates abnormal posture or exaggerated movements), chorea (abnormal involuntary movements such as jerking), athetosis (involuntary twisting or writhing)
managing parkinson’s: agonists and inhibitors ?
COMT inhibitors: entacapone. catechol-o-methyltransferase (COMT) enzyme metabolises levodopa in body and brain = entacapone taken with levodopa to slow breakdown = extends effective duration of levodopa
dopamine agonists: mimic dopamine in basal ganglia, stimulate dopamine receptors, less effective at reducing symptoms than levodopa (used to delay the use of levodopa) - prolonged use leads to pulmonary fibrosis. eg. bromocryptine, pergolide, cabergoline
monoamine
monoamine oxidase inhibitors: monoamine oxidase enzymes break down neurotransmitters eg. dopamine, serotonin, adrenaline. oxidase-b is specific to dopamine = inhibitors block enzyme leading to increase of dopamine circulating = used to delay levodopa use or in combo to reduced amount required. eg. selegiline, rasagiline
wtf is huntington’s ?
Autosomal dominant genetic condition (50% chance one parent will pass it on to children) causing progressive deterioration in the nervous system
patients usually asymptomatic until 30-50
trinucleotide repeat disorder - genetic mutation in HTT gene on chromosome 4
what is genetic anticipation ?
feature of trinucleotide repeat disorders eg. huntington’s
successive generations have more repeats in gene resulting in earlier age of onset and increased severity of the disease
how does huntington’s disease present?
insidious, progressive worsening of symptoms. usually begins with cognitive, psychiatric or mood problems followed by development of movement disorders
chorea (involuntary, abnormal movements)
eye movement disorders
dysarthria (speech difficulties)
dysphagia (swallowing difficulties)
diagnose huntington’s?
genetic test for the faulty gene, plus pre test and post test counselling regarding results
manage huntington’s ?
no treatment to slow/stop disease, key management is support
break bad news, involvement of MDT
antidepressants if depressed
QOL - occupational therapy, physiotherapy, psychological support
speech and lang therapy
genetic counselling - relatives and pregnancy
end of life care and advanced directives (document patients wishes before disease progresses)
medications for disordered movements: antipsychotics (eg. olanzapine), benzodiazepines (eg. diazepam), dopamine-depleting agents (eg. tetrabenazine)
prognosis of huntington’s?
progressive condition, life expectancy 15-20 years after onset of symptoms
as it progresses, patients less able to fight off illness/more susceptible
death often due to resp disease eg. pneumonia
suicide higher than in general population
differential diagnosis for headaches (it’s a long boi)
tension headaches, migraines, cluster headaches, secondary headaches, analgesic headache, hormonal headache
sinusitis
giant cell arteritis
glaucoma
inter cranial haemorrhage , subarachnoid haemorrhage
cervical spondylosis
trigeminal neuralgia
raised inter cranial pressure (brain tumours)
meningitis
encephalitis
wtf is a tension headache? + causes and treatment
very common, produced mild ache across forehead in band-like pattern, come on/resolve gradually, don’t produce visual changes
could be caused by muscle ache in frontalis, tempiralis or occipitalis muscles
associated with: stress, depression, alcohol, skipping meals, dehydration
treated with: reassurance, basic analgesia, relaxation, hot towel to local area
