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
wtf is a secondary headache? + causes
similar presentation to tension headache but clear cause secondary to: alcohol, head injury, carbon monoxide poisoning, underlying medical condition eg. infection, obstructive sleep apnoea, pre-eclampsia
wtf is sinusitis ? + treatment
headache associated with inflammation in ethmoidal, maxillary, frontal, or sphenoidal sinuses
causes facial pain behind the nose, forehead, eyes
tenderness over affected sinus
most sinusitis is viral hence usually resolves within 2-3 weeks
treatment: nasal irrigation with saline, prolonged symptoms treated with steroid nasal spray, antibiotics occasionally required
wtf is analgesic headache?
caused by long term analgesia use, similar features to tension headache, secondary to continuous or excessive analgesia use
withdrawal of analgesia treats headache but not always possible in patients with long term pain
wtf is a hormonal headache?
usually related to low oestrogen, generic non-specific tension-like headache
common: 2 days before & first 3 days of menstrual period, around menopause, during pregnancy (worse in first few weeks and improves in last 6 months - headaches in second half of pregnancy should be investigated for pre-eclampsia)
treat: oral contraceptive pill can improve headaches
wtf is cervical spondylosis ?
age-related degenerative changes/wear and tear affecting cervical spinal discs in neck
leads to neck pain (worse during movement) and often headaches
important to exclude spinal cord/nerve root lesions or other causes of neck pain eg. inflammation, malignancy, infection
wtf is trigeminal neuralgia ? + 3 branches of trigeminal nerve & treatment
nerve branches = ophthalmic (v1), maxillary (v2), mandibular (v3)
TN can affect any combo or branches - unclear cause but may be due to vascular compression of nerve
90% cases unilateral, 10% bilateral. 5-10% of people with MS have TN
presents: spontaneous, intense facial pain that can last seconds to hours, electricity-like shooting pain, attacks can worsen over time
triggers: cold weather, spicy food, caffeine, citrus
treatment: carbamazepine (anticonvulsant), surgery to decompress or intentionally damage trigeminal nerve
wtf is amaurosis fugax?
also known as transient monocular blindness
temporary loss of vision in one or both eyes, appears as black curtain coming down vertically into field of vision (dimming, fogging, blurring)
causes: embolus/plaque/clot obstructs the lumen of the retinal/ophthalmic artery = decrease in blood flow/stenosis
clot may have travelled from larger artery eg. carotid artery, artery in heart
may also be: head injury, brain tumour, migraine, blood vessel disease (polyarteritis nodosa), inflammation of optic nerve (optic neuritis), MS (inflam of nerves due to immune cells attacking NS), systemic lupus
wtf are cluster headaches ?
severe/unbearable unilateral headaches usually around the eye
clusters of 15 min - 3 hour long attacks, usually 3-4 a day for weeks/months followed by free period of 1-2 years
typical patient: 30-50 yr old male smoker
triggers: alcohol, strong smell, exercise
symptoms and treatment for cluster headaches?
symptoms: unilateral, extremely severe pain, red/swollen watering eye, miosis (pupil constriction), ptosis (eyelid drooping), nasal discharge, facial sweating
treatment: acute - triptans (eg. sumatriptan injected subcutaneously), high flow 100% oxygen for 15-20 mins
prevention/prophylaxis: verapamil, lithium, prednisolone (2-3 weeks to break cycle of clusters)
wtf are migraines? + types
complex neurological condition causing headaches and other associated symptoms, occur in attacks
migraine without aura, migraine with aura (eg. visual disturbance), silent migraine (with aura but without headache), hemiplegic migraine (weakness on one side of the body)
tend to get better over time and people often go into remission
symptoms of a migraine headache?
4-72 hours moderate to severe intensity pounding or throbbing usually unilateral but can be bilateral photophobia (discomfort with lights) phonophobia (discomfort with loud noise) nausea and vomiting with or without aura (visual changes eg. sparks, blurring, lines, loss of visual fields)
wtf is a hemiplegic migraine?
migraine mimics stroke (hence essential to act fast)
symptoms: typical migraine, sudden or gradual onset, hemiplegia (unilateral weakness or limbs), ataxia (disorders affecting coordination, balance, speech), changes in conciousness
possible triggers of migraines?
stress, bright lights, strong smells, certain foods (eg. chocolate, cheese, caffeine), dehydration, menstruation, abnormal sleep patterns, trauma
5 stages or migraines?
(some patients may only experience 1 or 2)
- premonitory/prodromal: 3 days before headache, subtle symptoms eg. yawning, fatigue, mood changes
- aura: lasting up to 60 mins
- headache: 4-72 hours
- resolution: headache can fade away or relieved completely by vomiting or sleeping
postdromal/recovery
management of migraines
acute: dark quiet room to sleep, medications - paracetamol, triptans (eg. sumatriptan), NSAIDs (eg. ibuprofen or naproxen), antiemetics if vomiting occurs (eg. metoclopramide)
triptans - 5HT/serotonin receptor agonists: abort migraines when they start to develop, act on smooth muscle in arteries causing vasoconstriction, peripheral pain receptors to inhibit activation of pain receptors, reduce neuronal activity in CNS
also: acupuncture, b2 supplements, NSAIDs for menstruation
prophylaxis/prevention: headache diary to track triggers, propranolol, amitriptyline, topiramate (can cause cleft palate so not for use during pregnancy)
wtf is dementia ?
acquired, progressive cognitive impairment disorder
involving one or more cognitive functions eg. memory, concentration, language, learning, praxis (learned motor acts), judgement, executive functions, social cognition
previous functional-level deterioration, consciousness remains
common causes of dementia? (mnemonic)
Diabetes Ethanol Medication Environmental (eg. CO poisoning) Nutritional (diets high in sugar, sat and trans fat) Trauma Infection Age
wtf is Alzheimer disease? + RF & pathophysio
most common cause of dementia
causes neurodegenerative loss of neutrons in cortex
mainly affects 65+
RF: down’s syndrome, ApoE E4 allele homozygosity, reduced cognitive activity, depression/loneliness
Path: extracellular deposition of beta-amyloid plaques, tau-containing intracellular neurofibrillary tangles, damaged synapses, atrophy
signs and symptoms of alzheimer’s ?
memory - episodic (recollection of experience) & semantic (recall words/concepts/numbers)
language (difficultly understanding/finding words)
attention and concentration issues
psychiatric changes eg. withdrawal, delusions
disorientation eg. time and surroundings
investigate and treat alzheimer’s ?
investigate: mini-mental state exam bloods - Thyroid function tests (TFTs), B12 (checking for other causes) memory clinic assessment MRI
treat:
no cure, medication to manage symptoms (AChE inhibitors eg. rivastigmine, galatamine, memantine), supportive therapy eg. carers and home changes
wtf is frontotemporal dementia? + RF & pathophysio
progressive dementia, atrophy of frontal and temporal lobes
5% of all dementias, more common in those under 65
RF: 50% dominant inheritance
Path: loss of neurons but no plaque formation, Tau positive or TDP-43 positive inclusions
signs and symptoms of frontotemporal dementia?
onset is insidious and progressive
3 main symptoms:
- behavioural issues eg. loss of inhibition/empathy, compulsive, can’t plan
- progressive aphasia eg. slow difficult speech, grammatical errors
- semantic dementia eg. loss of vocabulary, problems understanding
investigate and treat frontotemporal dementia?
investigate: bloods (b12, tfts, u&es), fbc and lfts for suspected encephalopathy, mini-mental state exam, mri to look at atrophy
treat: no cure, SSRIs (antidepressants for behaviour symptoms) supportive therapy (eg. speech and lang, carers, home changes, help set up routine), levodopa/carbidopa if parkinson’s symptoms present, stop exacerbating drugs
wtf is vascular dementia? + RF & pathophysio
second most common globally, 17% of dementia in UK
result of multiple small infarcts (tissue death due to lack of blood supply)
RF: smoking, history of TIAs, AF, hypertension, DMT1, hyperlipidaemia, obesity, coronary heart disease, 1 stroke = double risk of VD
Path: based on location and size of original infarct & number/location of consequent infarcts
signs and symptoms of vascular dementia?
‘stepwise progression’ = periods of stable symptoms followed by sudden increase in severity
presentation has huge variation but can include: visual disturbances, UMN signs (eg, muscles weakness, overactive reflexes, clonus - involuntary and rhythmic muscle contractions), attention deficit, depression, incontinence, emotional disturbances
if infarct subcortical (deep within brain eg. basal ganglia) = dysarthria (slurring) and parkinsonisms
investigate and treat vascular dementia?
investigate: full history (previous stroke/tia?), cognitive impairment screen, medication review, MRI (look for previous infarcts)
treat: supportive therapy eg. carer, home changes, cognitive stimulation programmes), SSRIs or antipsychotics to control symptoms eg. lorazepam
prognosis = 3-5years from diagnosis
symptoms, investigate and treat dementia with lewy bodies?
associated symptoms: visual hallucinations, delusions, disorders of REM sleep (rapid eye movement), restless leg syndrome, fluctuating consciousness, parkinsonisms eg. tremor, rigidity, shuffling gait
investigate: dementia with 2 of = recurrent visual hallucinations, spontaneous parkinsonisms, fluctuating concentration/attention
SPECT/PET scan showing low dopamine transporter upstate in basal ganglia
MMSE, bloods
treat: cholinesterase inhibitors eg. rivastigmine for cognitive decline
avoid neuroleptic drugs eg. haloperidol = severe sensitivity reactions
