Neurology Flashcards
1
Q
Craniotomy
A
Removing part of bone from skull to expose brain eg. to remove tumour. Bone flap is temporarily removed and then immediately replaced after brain surgery.
2
Q
Craniectomy
A
Portion of skull removed to help relieve pressure on brain. Bone fragment not immediately put back into place but rather kept (eg in abdomen to keep the tissue alive) and then replaced in a future surgery once pressure recovers. Occasionally bone fragment is simply discarded.
3
Q
Aphasia
A
- Impairment of language, affecting the production or comprehension of speech and the ability to read/write.
- Often due to stroke but can also arise from other brain injuries eg. head trauma, tumours, infection.
- Can be temporary or permanent
4
Q
Global aphasia
A
- most severe type of aphasia
- patients ca produce few recognisable words and understand little or no spoken language
- Cannot read or write
5
Q
Broca’s aphasia
A
- Non-fluent aphasia
- Speech output is severly reduced and limited, vocabulary is limited and formation of sounds is laborious and clumsy. Patient often halts during speech
- Patient may understand speech well and can read but be limited in writing
- Often complains that they can’t “find the words”
6
Q
Mixed non-fluent aphasia
A
- Sparse and effortful spech, resembling sever Broca’s aphasia
- However, unlike Broca’s, they struggle to understand spech and cannot read or write
7
Q
Wernicke’s aphasia
A
- Fluent aphasia
- Cannot grasp meaning of spoken words
- Can still produce connected speech but sentences do not make sense and often include irrelevant words which don’t make sense together
- Reading and writing often impaired
8
Q
Myasthenia gravis, it symptoms an risk factors
A
- Chronic autoimmune disorder of post-synaptic membrane at NMJ in skeletal muscle
- Characterised by muscle weakness- increases during exercise, improves on rest (muscle strength fatigability)
- Commonly presents with ptosis, diplopia, oropharyngeal (dysphagia) and appendicular (limb) weakness and SOB
- Risk factors- family history of autoimmune disorders, genetic markers, cancer-targeted therapy
9
Q
Myasthenia gravis- pathophysiology and investigations
A
- Circulating antibodies against the nicotinic acetylcholine receptor (AChR) or associated proteins impair neuromuscular transmission
- Elevated serum levels of antibodies against AChR or muscle-specific tyrosine kinase (MuSK) usually present (serum antibody analysis)
- Could also have antibodies against LRP4, collagen Q and cortactin
- Clinical electrophysiology results include decrease in response on repetitive nerve stimulation
- Could also perform serial pulmonary function tests
10
Q
Myasthenia gravis- treatment
A
- Pyridostigmine (anticholinesterase inhibitor)
- Immunotherapy (corticosteroid, immunosuppressants), efgartigimod alfa
11
Q
Myasthenic crisis
A
Exacerbation necessitating mechanical ventilation and acute treatment with IV immunoglobulin or plama exchange
12
Q
Acetylcholine
A
- excitatory neurotransmitter
- main neurotransmitter of the parasympathetic nervous system
13
Q
Alzheimer’s disease and presentation
A
- Chronic, progressive neurodegenerative disorder
- Characterised by a global, non-reversible impairment in cerebral functioning
- Deteriotating course over 8-10 years
14
Q
Alzheimer’s disease symptoms and risk factors
A
- Memory loss, disorientation, slight dysphasia, mood changes, constructional dyspraxia, prospagnosia (inability to recognise faces)
- Risk factors- advanced age, family history, genetics, DOwn’s syndrome
- May co-exist wtith vascular dementia= mixed ementia
15
Q
Alzheimer’s disease- investigations
A
- Bedside cognitive testing: MMSE is standard (but take into account education and language), MoCA (fast but limited as it only detects MCI)
- FBC- rules out anaemia
- Metabolic panel- excludes abnormal sodium, calcium, glucose
- Serum TSH- rules out hyperthyroid or hypothyroid-associated dementia
- Serum B12- rules out vitamin B12 deficiency-induced dementia
- Urine drug screen- rules out recreational drug use
- CT- excludes tumours, vascular disease etc
- MRI- may display generalised atrophy with medial temporal lobe and later parietal predominance associated with the disease
16
Q
Alzheimer’s disease- treatment
A
- Supportive treatment- care support
- (Anti)cholinesterase inhibitor eg donepezil
- Switch to or add memantine in severe disease (NMDA antagonist)
17
Q
Alzheimer’s disease- pathophysiology
A
- brain lesions marked by neurofibrillatory tangles, senile plaques, neuronal loss and brain atrophy, with defects in acetylcholine synthesis at cellular level
18
Q
Vestibular schwannoma
A
- aka acoustic neuroma
- benign, slow-growing tumour
- results from overproduction of Schwann cells (myelinating cells) of the vestibular and/or cochlear nerves supplying the inner ear
- symptoms usually include unilatearl hearing loss, tinnitus and dizziness/loss of balance
- Larger tumours may affect the trigeminal nerve= facial numbness.
19
Q
Horner’s syndrome and symptoms
A
- 4 classic signs of the disorder:
- miosis (constricted pupil)
- ptosis (drooping of upper eyelid)
- anhidrosis (absence of sweating of the face)
- enophthalmos (sinking of eyeball into bony cavity)
- Symptoms tend to be unilateral, all on the same side
20
Q
Horner’s syndrome- causes
A
- congenital (rare)- present at birth
- carotid artery dissection (“painful Horner’s”, 4 symptoms + headache of acute onset is pathognomic of carotid dissection. Hypoglossal nerve most commonly affected, diagnosed on MRI and MRA)
- Tumour in neck/chest/lungs
- lesion in brain/upper spinal cord/neck/eye orbit
- If Horner’s caused by lesion.tumour surgical treatment/radiation may treat it.
- Physical findings of Horner’s develop due to interruption of sympathetic nerve supply to the eye.
- Idiopathic Horner’s= no apaarent reason/unknown cause
21
Q
Parkinson’s disease
A
- Progressive disorder caused by degeneration of nerve cells in the substantia nigra- these nerves conrol movement
- The nerve cells in the substantia lose the baility to produce dopamine
22
Q
4 hallmark symptoms of Parkinson’s disease
A
- Bradykinesia (slowness of movement)
- tremor
- rigidity
- impaired balance and coordination (postural instability)
23
Q
Causes of Parkinson’s disease
A
- Unknown but thought to do with oxidative damage, environmental toxins, genetic gactors and accelerated aging
24
Q
Parkinson’s disease- investigations
A
- No x-ray or blood test available
- Typically diagnosed by presence of 2 of the 3 primary symptoms with absence of other neurological signs upon examination
- Patient should have no history of other possible causes of parkinsonism eg. tranquiliser medicaitons, head trauma, stroke
- Improvement of symptoms in response to Levodopa and other parkinson’s medications confirms diagnosis
25
What are Parkinson-Plus syndromes?
* aka disorders of multiple system degeneration or secondary/ atypical Parkinsonian
* These syndromes have the classical motor features of Parkinson's disease plus additional features that distinguish them from idiopathic Parkinson's disease
* Usually difficult to differentiate between idiopathic Parkinson's and Parkinson's-plus but dopaminergic medicines ef Levodopa, are generally effective in people with primary disease but not in those with secondary parkinsonism.
26
What are some examples of Parkinson-Plus syndromes
* Progressive Supranuclear Palsy (PSP)
* Corticobasal syndrome (CBS)
* Multiple System Atrophy (MSA)
27
Which dementia is associated with Parkinson's
Lewy body dementia (2 types depending on order of symptoms):
- Parkinson's dementia
- Dementia with Lewy bodies
28
Tonic-clonic seizures
* involve both tonic (stiffening)
* and clonic (twitching or jerking) phases of muscle activity
29
Wernicke encephalopathy and it's 3 main symptoms
* acute neurological condition
* life threatening
* characterised by ophthalmoparesis (paralysis/weakness of eye muscles) with nystagmus, ataxia and confusion
30
Wernicke encephalopathy causes
* thiamine (B1) deficiency primarily affecting the peripheral and central nervous symptoms
31
Sodium valporate
* used to treat epilepsy and bipolar disorder
* should not be used in pregnancy
32
Hydrocephalus
* accumulation of excess CSF in ventricles of brain
* excess fluid leads to increased intracranial pressure
33
Non-communication (obstructive) hydrocephalus
* Flow of CSF blocked along one or more passages connecting the ventricles- causes enlargement of pathways upstream of block= increased ICP
34
Cerebrospinal fluid (CSF) functions
1. "shock absorber" surrounding brain and spinal cord
2. delivers nutrients to brain and removes waste from it
3. flows between cranium and spine to regulate changes in pressure
35
Causes of CSF accumlation
## Footnote
CSF accumulation is bad as raises ICP and exerts pressures on brain tissues in skull
* increase in production of CSF
* decrease in CSF absorption
* blockage of normal CSF flow in ventricular system
36
Communicating hydrocephalus
* no obstruction to flow of CSF in ventricular system
* either due to inadequate absorption or abnormal increase in quantity of CSF produced
37
Acquired hydrocephalus
* typically caused by injury/disease at any age
38
Congenital hydrocephalus
* present at birth
* may be caused by events that occur during fetal development or as result of genetic abnormalities
39
Normal pressure hydrocephalus
* more common in elderly
* dilated ventricles with normal pressure within spinal column
40
Hydrocephalus ex vacuo
* compensatory enlargement of CSF spaces
* increase in CSF volume, enlarged cerebral ventricles and subarachnoid spaces
* caused by brain (encephalic volume loss)
