Neurology 🧠Flashcards
(208 cards)
1
Q
What is the most common cause of dementia?
A
Alzheimer’s
2
Q
What are the risk factors for Alzheimer’s disease?
A
-age
-genetics (mutations in APP, PSEN1, PSEN2, APOE)
-cardiovascular disease
-depression
-low educational attainment
-low social engagement & support
-head trauma
-learning difficulties
3
Q
What are the pathological changes seen in Alzheimer’s disease?
A
-beta-amyloid plaques (extracellular)
-neurofibrillary tangles (intracellular)
4
Q
Where in the brain are beta-amyloid plaques & neurofibrillary tangles deposited in Alzheimer’s disease?
A
hippocampus & medial temporal lobes
5
Q
What are the clinical features of Alzheimer’s disease?
A
-cognitive impairment
-behavioural and psychological symptoms (BPSD)
-early memory impairment & difficulty learning new information
-difficulties with activities of daily living
6
Q
What are the cognitive domains assessed using cognitive assessment tools?
A
-attention & concentration
-memory
-language
-praxis (planned motor movement)
-executive function
-visuospatial function
7
Q
What are the differential diagnoses for Alzheimer’s disease?
A
-depression (& other psychiatric disorders)
-drugs (especially anti-cholingergics)
-delirium
8
Q
What are the diagnostic criteria for Alzheimer’s disease?
A
-functional ability
-cognitive remains (impairment involving 2+ cognitive domains)
-exclusion of differentials
9
Q
What is mild cognitive impairment?
A
When there is a deficit in a single domain (of the dementia diagnosis areas) and it is mild.
10
Q
What are the investigations for Alzheimer’s disease?
A
-full bloods to exclude other diagnoses
-ECG, syphilis testing, CXR
-neuroimaging (typically MRI)
11
Q
What is the non-pharmacological management of Alzheimer’s disease?
A
-assess capacity & advanced care planning
-inform DVLA
programmes to improve/maintain cognitive function
-managing BPSD
-care plans
-end-of-life care
12
Q
What is the pharmacological management of Alzheimer’s disease?
A
mild-to-moderate AD: acetylcholinesterase inhibitors (donepezil, rivastigmine)
moderate-to-severe: memantine
13
Q
What is Bell’s palsy?
A
idiopathic unilateral facial nerve palsy causing unilateral facial weakness
14
Q
What are the functions of the facial nerve?
A
-supplies stapedius muscle within ear
-muscles of facial expression
-parasympathetic supply to lacrimal & salivary glands
-provides taste to anterior 2/3 of tongue
15
Q
What is the most common cause of facial nerve palsy?
A
Bell’s palsy
16
Q
What are the clinical features of Bell’s palsy?
A
-rapid onset unilateral facial weakness (<72h)
-post-auricular/ear pain
-difficulty chewing
-incomplete eye closure
-drooling
-tingling
-hyperacusis (heightened sensitivity to sound)
-loss of nasolabialfold
-drooping of eyebrow
-drooping corner of mouth
-asymmetrical smile
-Bell’s sign (upward movement of the eye maintained on attempt to close the eye)
17
Q
How do you differentiate between Bell’s palsy & stroke?
A
strokes are forehead sparing, Bell’s palsy causes forehead paralysis
18
Q
What does the House-Brackmann system assess?
A
degree of facial nerve damage/paralysis following surgery or Bell’s palsy
19
Q
How is Bell’s palsy diagnosed?
A
-clinical diagnosis based on unilateral facial weakness, rapid onset, no forehead sparing
-blood test, neuroimaging, HIV test to exclude other causes (incl. Ramsay-Hunt)
20
Q
What is the management of Bell’s palsy?
A
-largely supportive
-prednisolone if presenting within 72h of onset (50mg for 10 days)
21
Q
What is the prognosis of Bell’s palsy?
A
most patients will fully recover within 4 months
22
Q
What is a cluster headache?
A
-severe primary recurrent unilateral headaches around the eye or temporal region
-last 15min to 3h
23
Q
What are the diagnostic criteria for cluster headaches?
A
-at least 5 attacks
-severe, unilateral orbital/temporal pain lasting 15-180 mins
-associated with one of the following on the ipsilateral side; conjunctival infection, nasal congestion, eyelid oedema, forehead sparing, facial sweating, mitosis/ptosis
-restlessness/agitation
-occurring every 2 days up to 8 per day
24
Q
What are the 2 subtypes of cluster headaches?
A
-episodic: pain-free intervals of at least 3 months between clusters
-chronic: do not have a period of remission lasting longer than 3 months
25
What are the red flag characteristics in headaches?
-severe sudden onset
-progressive or persistent, acute change
-worse on standing
-worse on lying
26
What are the investigations for cluster headaches?
-neurology review
-MRI and CT to exclude other causes
27
What is the management of cluster headaches?
-sumatriptan
-trigger avoidance
-traditional analgesia
-short burst oxygen therapy
-verapamil as preventative
28
What is delirium?
an acute confusional state that causes disturbed consciousness, attention, cognition & perception
29
What are the characteristic features of delirium?
-acute onset
-symptoms fluctuate throughout the day
-altered awareness & attention
-disturbed cognition
-evidence of organic cause
30
What are the 3 subtypes of delirium?
-hyperactive: agitation, restlessness, hallucinations
-hypoactive: lethargic, withdrawn, drowsy
-mixed delirium
31
What are the risk factors for delirium?
-age
-multiple comorbidities
-frailty
-malnutrition
-visual/hearing impairment
-functional impairment
-alcohol excess
-major injury e.g. hip fracture
-cognitive impairment
32
What is the diagnostic criteria for delirium?
-disturbance in awareness & attention
-acute onset, acute change from baseline & fluctuant
-disturbance in cognition
-not better explained by another neurocognitive disorder
-evidence of an organic cause
33
What is the management of delirium?
-address underlying cause
-mental capacity assessment
-rapid tranquillisation may be required (benzodiazepines, anti-psychotics)
34
What are the options for rapid tranquillisation in delirium?
-benzodiazepines: lorazepam
-anti-psychotics: haloperidol, olanzepine
35
What are the 2 stages of assessing capacity?
1. does the person have an impairment of the mind or brain, as a result of illness or external factors (drugs/alcohol)?
2. does the impairment mean the person is unable to make a specific decision when they need to?
36
What are the main causes of dementia?
-Alzheimer's disease (50-70%)
-vascular dementia (20%)
-Lewy-body dementia (15-20%)
-frontotemporal dementia (2%)
-rarer causes: Parkinson's, Huntington's
37
What are the behavioural and psychological symptoms of dementia (BPSD)?
-agitation & emotional lability
-depression & anxiety
-sleep cycle disturbance
-disinhibition
-withdrawal/apathy
-motor disturbance
-psychosis
38
What are the main features of vascular dementia?
-stepwise decline in function
-predominant gait, attention & personality changes
-may have focal neurological signs (previous stroke)
39
What are the main features of Lewi-body dementia?
-Parkinsonism
-falls, syncope
-hallucinations
40
What are the main features of frontotemporal dementia?
-marked personality change
-behavioural disturbances
-memory and perception relatively preserved
41
How is the severity of dementia assessed?
-MMSE
-MoCA
-clinical dementia rating (CDR)
42
How is the severity of dementia categorised?
Mild: MMSE 21-26, MoCA 18-25, CDR 1
Moderate: MMSE 10-20, MoCA 10-17, CDR 2
Severe: MMSE <10, MoCA <10, CDR 3
43
What is the pharmacological management of dementia?
-acetylcholinesterase inhibitors (donepizil, rivastigmine)
-memantine
44
What is encephalitis?
inflammation of the brain parenchyma, which characteristically presents with abnormal brain function
45
What is the most severe cause of encephalitis?
herpes simplex virus encephalitis - usually fatal without treatment
46
What are the possible causes of encephalitis?
infectious: can be viral, bacterial, fungal, parasitic
non-infectious: paraneoplastic, post-infectious, autoimmune
47
What are the features of HSV encephalitis?
-HSV1: rapid onset fever, headache, altered mental status, seizures, neurological deficits
-can cause CNS infection by invasion following oropharyngeal infection, or reactivation of dormant virus
-damage is typically within the temporal lobes
48
What are the features of post-infective encephalitis?
-immune mediated disorder usually seen in children
-demyelinating condition
-development of encephalopathy 4-13 days following an infection or vaccination
-due to development of antibodies against components of myelin
49
What are the features of autoimmune encephalitis?
-immune-mediated inflammatory disorders of the brain tissue
-antibody develops against an antigen within the CNS
-this initiates an immune response which leads to encephalitis
-e.g. NMDA encephalitis: antibody targets the NMDA receptor
50
What are the features of paraneoplastic encephalitis?
-due to the immune system reacting to antigens expressed on the tumour and the nervous system
specific cancers have been linked to specific autoantibodies:
-limbic encephalitis
-brainstem encephalitis
-antibody related syndrome
51
What are the clinical features of encephalitis?
-fever
-headache
-altered mental status
-focal neurological deficits
-seizures
52
What investigations are important in encephalitis?
-neuroimaging
-EEG
-CSF analysis: protein, viral PCR, MC&S, glucose, serology
-serological testing
53
What is the management of encephalitis?
-infective causes: antimicrobials
HSV encephalitis: IV aciclovir
-paraneoplastic, autoimmune & post-infective causes: immunosuppressive e.g. steroids
54
What is a seizure?
transient neurological change due to synchronous, hyper excited neuronal activity in the brain
55
What is the aetiology of epilepsy?
-genetic
-structural abnormalities
-metabolic disorders
-immune disorders
-chronic infections
-unknown
56
What is the pathophysiology of epilepsy?
-imbalance between inhibitory & excitatory signals
-gabanergic = inhibitory
-glutametergic = excitatory
57
What are the risk factors for epilepsy?
-cerebrovascular disease
-head trauma
-cerebral infections
-family history
-premature birth
-congenital malformations of the brain
-genetic conditions associated with epilepsy
58
What are the different types of seizures?
-area of onset: focal, general, focal to bilateral tonic-clonic
-awareness: aware, impaired awareness
-motor: tonic, clonic, myoclonic, atonic, spasms
-non-motor: absence, sensory, emotional, autonomic or behavioural changes
59
What are the different types of epilepsy?
-focal epilepsy
-generalised epilepsy
-generalised & focal epilepsy: combination of both
-unknown epilepsy: insufficient evidence to conclude whether focal, generalised, or both
60
What are the 4 stages of a seizure?
-prodrome: feeling or sensation occurring before the onset of a seizure
-early ictal: characterised by an aura, suggestive of focal epilepsy
-ictal phase: depends on seizure type, tonic-clonic movements, urinary incontinence, tongue biting
-post ictal: recover period once the seizure has finished
61
What are the diagnostic criteria for epilepsy?
any of the following:
-2+ unprovoked seizures occurring more than 24h apart
-1 unprovoked seizure with a probability of further seizures felt to be at a similar recurrence risk to patients with 2+ unprovoked seizures over the next 10 years
-a diagnosed epilepsy syndrome
62
What are the differential diagnoses for epilepsy?
-syncope & anoxic seizures
-behavioural, psychological & psychiatric
-sleep-related conditions
-paroxysmal movement disorders
-migraine associated disorders
63
What are the investigations for epilepsy?
-EEG: supports a diagnosis of epilepsy & determines seizure type
-MRI/CT: structural abnormalities
64
What are the key aspects of epilepsy management?
-education & safety
-treating acute seizures
-long term treatment with anti epileptics
65
What are the safety precautions in epilepsy?
-driving: depends on type of license & type of seizure
-water safety: showers instead of baths
-fire safety: caution with heat/flames
-environmental safety: home/work environment
-other: heights, contraception, high risk activities
66
What are the common anti epileptic drugs?
-sodium valproate
-carbamazepine
-lamotrigine
-levetiracetam
-phenytoin
67
What are the key points about sodium valproate?
-unclear mechanism
-teratogenic
-SEs: liver injury, pancreatitis, increased suicide risk
68
What are the key points about carbamazepine?
-sodium channel antagonist
-increased teratogenic risk
-SEs: agranulocytosis, SIADH
69
What are the key points about lamotrigine?
-sodium channel antagonist
-SEs: severe skin reactions
70
What are the key points about levetiracetam?
-unclear mechanism
-SEs: CNS disturbances (somnolence, decreased energy, headache), neurophsychiatric disturbance
71
What are the key points about phenytoin?
-sodium channel antagonist
-teratogenic
-SEs: arrhythmia with parenteral use, gum hypertrophy, cerebellar atrophy
72
What is the pharmacological management of focal seizures?
1st line - Lamotrigine (if childbearing potential), alternative carbamazepine (if no childbearing potential)
2nd line - Levetiracetam, oxcarbazepine or sodium valproate
73
What is the pharmacological management of generalised tonic-clonic seizures?
1st line - sodium valproate* or lamotrigine.
2nd line - clobazam, lamotrigine, levetiracetam or topiramate
74
What is the pharmacological management of absence seizures?
1st line - ethosuximide or sodium valproate*.
2nd line - lamotrigine
75
What is the pharmacological management of myoclonic seizures?
1st line - sodium valproate.
2nd line - levetiracetam or topiramate
76
What is the pharmacological management of juvenile myoclonic epilepsy?
1st line - sodium valproate*.
2nd line - lamotrigine , levetiracetam or topiramate
77
What is an essential tremor?
a tremor during voluntary muscle contratction, is brought out by anti-gravity positions (e.g. outstretched hands)
78
What is the cause of essential tremor?
-associated with strong family history
-suspected to be autosomal dominant
-exact mechanism not understood
79
What are the clinical features of an essential tremor?
-usually bilateral
-occurs on movement/outstretching of the arms
-most commonly affects the hands & arms
-typically high frequency with low amplitude
-improves slightly with alcohol
-usually no other neurological signs
80
How is a diagnosis of essential tremor made?
clinical diagnosis based on:
-isolated upper limb action tremor
-with/without tremor in other sites (e.g. head)
-duration >3 years
-no other neurological features
81
What is the pharmacological management of essential tremor?
propranolol (beta blocker) or primidone (anti-epileptic)
82
What are the non-pharmacological management options for essential tremor?
-neuromodulation
-botox injections
-deep brain stimulation
83
What is frontotemporal dementia?
-focal degeneration of frontal & temporal lobes
-disturbances is social behaviour, personality & language
-typically affects patients at a younger age (average 58)
84
What are the 3 subtypes of frontotemporal dementia?
-behavioural variant: most common, personality & behaviour change
-non-fluent primary progressive aphasia: articulatory difficulty
-semantic primary progressive aphasia: impaired single-word comprehension
85
What is the aetiology of frontotemporal dementia?
strong genetic predisposition: MAPT, GRN, C90RF72 gene
86
What is the pathophysiology of frontotemporal dementia?
-degeneration of frontal/temporal lobes
-deposition of abnormal proteins e.g. tau proteins, Pick bodies
87
What are the clinical features of FTD (behavioural variant)?
-disinhibition
-loss of empathy
-apathy
-hyperorality (e.g. dietary changes, consuming non-edible products)
-compulsive behaviour
88
What are the clinical features of FTD (primary progressive aphasia variant)?
-effortful speech
-halting speech
-speech-sound errors
-speech apraxia
-difficulty finding words
-surface dyslexia or dysgraphia (mispronouncing difficult words)
89
What are the motor syndromes associated with FTD?
-FTD with motor neurone disease
-corticobasal syndrome: rare neurogenerative disorder
-progressive supranuclear palsy
90
What are the pharmacological management options for FTD?
medications to manage behavioural/cognitive dysfunction e.g.:
-SSRIs
-atypical antipsychotics
91
What is the prognosis of frontotemporal dementia
overall survival is 8-10 years from symptom onset
92
What is Guillain-Barré syndrome?
-acute, inflammatory polyneuropathy
-progressive ascending weakness of the lower limbs
-majority of patients have a preceding illness (gastroenteritis or flu)
93
What are the common triggers of Guillain-Barré syndrome?
-campylobacter (25-50%)
-other infection: CMV, EBV, hepatitis E, mycoplasma pneumoniae
94
What is the pathogenesis of Guillain-Barré syndrome?
-immune-mediated damage to peripheral nerves
-demyelination
95
What are the key investigations for suspected Guillain-Barré syndrome?
-electromyography
-nerve conduction studies
-lumbar puncture: high protein, normal WCC
-spirometry: to measure involvement of respiratory muscles
96
What is the management of Guillain-Barré syndrome?
-plasma exchange or IV immunoglobulin quickens recovery
-supportive care: analgesia, respiratory support, DVT prophylaxis
97
What is the Hughes disability score used for?
functional assessment of patients with Guillain-barre syndrome
98
What are the factors associated with poorer prognosis in Guillain-barre syndrome?
-old age
-preceding campylobacter infection
-rapid onset and severe presenting symptoms
-need for mechanical ventilation
99
What is the triad of features in Horner's syndrome?
unilateral:
-miosis (pupil constriction)
-ptosis
-anhidrosis
100
What is the pathophysiology of Horner's syndrome?
lesion along the oculosympathetic pathway, which is a sympathetic pathway responsible for:
-pupil dilatation
-sweating
-eyelid elevation
101
What are possible causes of Horner's syndrome?
-stroke
-space occupying lesion
-multiple sclerosis
-syringomyelia (fluid-filled spinal cord cyst)
-trauma
-pancoast tumour
-thoracic outlet syndrome
-thoracic aneurysm
-carotid artery dissection
-cavernous sinus pathology
-neck mass
102
What are the neurological features associated with Horner's syndrome?
-brainstem signs: diplopia, vertigo, ataxia, focal weakness
-spinal cord signs: weakness, sensory level, bowel & bladder impairment
-axillary or lung apex involvement: arm pain, hand weakness
-isolated Horner's: concerning for carotid dissection
103
What are the investigations in Horner's syndrome?
-CT angiography to exclude carotid artery dissection
-MRI for suspected spinal cord lesions
-CT chest for suspected pan coast tumour
104
How is Horner's syndrome diagnosed?
-cocaine drops: fails to cause pupil dilatation
-apraclonidine drops: causes exaggerated pupil constriction
105
What is Huntington's disease?
-autosomal dominant neurodegenerative condition
-characterised by chorea, dystonic & cognitive changes
-onset around 30-50 years
-caused by CAG triplet repeats
106
What are the motor features of Huntington's disease?
-chorea: abnormal, abrupt, involuntary movements
-dysphagia & speech difficulties
-dystonia: muscle spasms & contractions
-parkinsonian features: bradykinesia, rigidity
107
What are the psychiatric features of Huntington's disease?
-mood changes: often precede motor symptoms
-depression & increased suicide risk
-paranoia, delusions, irritability, agitation, sleep disturbance
108
What are the cognitive features of Huntington's disease?
-affects ability make complex decisions & multitask
-memory loss & dementia may develop
109
How is Huntington's disease diagnosed?
PCR analysis/gel electrophoresis to identify the number of CAG repeats
110
What is the pharmacological management of Huntington's disease?
-dopamine depleting agents (e.g. tetrabenazine): helps with chorea, but may result in Parkinsonism
-antipsychotics (e.g. risperidone)
-benzodiazepines (e.g. clonazepam)
111
What is the prognosis of Huntington's disease?
normally fatal 15-20 years after symptom onset
112
What are the risk factors for IIH (idiopathic intracranial hypertension)?
-increased weight
-female
-reproductive age
113
What are the medications/conditions associated with IIH?
-medications: GH, tetracyclines, retinoids
-excess vitamin A
-systemic illness: sleep apnoea, hyper coagulable disorders, PCOD, SLE, Behcet's syndrome, endocrine disorders
114
What are the potential mechanisms behind IIH?
-venous sinus narrowing/stenosis
-central obesity
-altered sodium & water retention
-impaired CSF reabsorption
115
What are the clinical features of IIH?
-headache: worse lying down/bending over
-papilloedema
-visual changes: diplopia, flashes, transient visual loss, 6th nerve palsy
116
How is IIH diagnosed?
-exclude structural causes of raised ICP with neuroimaging
-raised pressures on lumbar puncture
Dandy criteria:
-typical symptoms
-absence of additional neurological features
-raised ICP with normal CSF composition
-absence of other causes of intracranial HTN
117
What are the differential diagnoses of IIH?
-space occupying lesion
-venous outflow obstruction
-obstructive hydrocephalus
-decreased CSF reabsorption
-increased CSF production (choroid plexus papilloma)
118
What are the different causes of optic disc swelling?
-papilloedema (raised ICP)
-optic nerve pathologies (optic neuritis)
-retinal artery or vein occlusion
-uveitis
119
What is the management of IIH?
-weight loss
-carbonic anhydrase inhibitors (e.g. acetazolamide)
-surgical treatment: optic nerve sheath fenestration, shunting
120
What is the main complication of IIH?
permanent visual loss
121
What the pathophysiology of Lewy body dementia?
presence of Lewy bodies in the cerebral cortex & brainstem
122
Which genetic mutations are associated with Lewy body dementia?
SNCA, PSEN1/PSEN2, APOE, APP
123
What are the characteristic features of Lewy body dementia?
-fluctuating cognition
-visual hallucinations
-Parkinsonism (bradykinesia, rest tremor, rigidity)
-REM sleep disorders: may precede cognitive decline
124
What are the clinical features that support a diagnosis of Lewy body dementia?
-severe sensitivity to antipsychotic agents
-postural instability & repeated falls
-syncope
-severe autonomic dysfunction (constipation, orthostatic hypotension, incontinence)
-excessive daytime sleepiness
-decreased sense of smell
125
What is the specialist neuroimaging that supports a diagnosis of Lewy body dementia?
-SPECT: looks at dopamine uptake
-polysomnography: assesses for REM sleep disorders
-EEG, MRI
126
What are the pharmacological interventions for Lewy body dementia?
-cholinesterase inhibitors (rivastigmine, donepezil)
-memantine
-antipsychotics (e.g. quetiapine)
-melatonin (for REM sleep disorders)
-levodopa
127
What is the prognosis of Lewy body dementia?
-mean survival is 6.1 years
-features with worse prognosis: cognitive fluctuations, early hallucinations, gait abnormalities
128
What is the difference between chronic migraine & episodic migraine?
-chronic: headache on more than 15 days each month, 8 of which have features of migraine
-episodic: less frequent than above
129
What are the typical features of migraines?
-attacks last 4-72 hours
-unilateral
-pulsating
-moderate/severe intensity
-aggravated by physical activity
-associated with nausea/photophobia/phonophobia
-may be associated with aura (neurological symptoms preceding headache)
130
What are red flags when differentiating between migraine and TIA/stroke?
-motor weakness
-diplopia
-visual symptoms affecting only one eye
-poor balance
-decreased level of consciousness
131
What is the acute management of migraines?
-simple analgesia (paracetamol, ibuprofen, aspirin)
-triptans
-antiemetics
132
What are the preventative options in migraine?
-propranolol
-topiramate (contraindicated in pregnancy)
-amitriptyline
-galcenezumab
133
What is the pharmacological management for menstrual-related migraine?
-frovatriptan
-zolmitriptan
134
What are the complications associated with migraines?
-status migraine: persists for over 72 hours
-persistent aura without infarction: lasting over 1 week
-migrainous infarction: cerebral infarction occurs during aura
-migraine aura-triggered seizure
-ischaemic stroke
135
What is a mononeuropathy?
-damage/dysfunction of a single peripheral nerve
-leads to motor and/or sensory dysfunction
-commonly due to entrapment or compression
136
What are the functions of visceral fibres in the PNS?
-visceral sensory fibres: carry signals from thoracic & abdominal compartments
-visceral motor fibres:form the autonomic nervous system (sympathetic & parasympathetic)
137
What are the functions of somatic fibres in the PNS?
-sensory input from skin, muscles, bones & joints
-motor output to glands & muscles
138
What are the 3 broad groups of mononeuropathies?
-cranial
-upper limb
-lower limb
139
What are the main nerves of the upper limb?
-median
-ulnar
-radial
-axillary
-other: musculocutaneous, long thoracic, suprascapular, spinal accessory
140
What are the main nerves of the lower limb?
-common peroneal
-tibial
-femoral
-sciatic
-other: sural, obturator, lateral cutaneous nerve of the thigh
141
What are the 12 cranial nerves?
-CN I: olfactory
-CN II: optic
-CN III: oculomotor
-CN IV: trochlear
-CN V: trigeminal
-CN VI: abducens
-CN VII: facial
-CN VIII: vestibulocochlear
-CN IX: glossopharyngeal
-CN X: vagus
-CN XI: accessory
-CN XII: hypoglossal
142
What are the possible causes of peripheral nerve injury?
-compression (e.g. compartment syndrome, carpal tunnel)
-transection (usually due to trauma)
-inflammation
-ischaemia (due to vasculitis, atherosclerosis, DM)
-radiation
143
What is the path of the median nerve?
-derived from brachial plexus (C5-T1)
-travels alongside the brachial artery into the cubital fossa
-travels along forearm, through carpal tunnel
144
Which nerve is affected in carpal tunnel syndrome?
median
145
What is the sensory function of the median nerve?
sensory innervation to the palmar & distal dorsal aspects of the lateral 3 1/2 digits & central palm
146
What are the motor functions of the median nerve?
-in the forearm: pronator trees, FCR, PL, FDS, pronator quadrates, FPL, part of FDP
-in the hand: thenar eminence & 2 lateral lumbricals
147
What are the causes/risk factors for carpal tunnel syndrome?
-risk factors: DM, pregnancy, RA, obesity, thyroid disease
-other causes: haematoma, trauma, tumour, vasculitis
148
What are the clinical features of carpal tunnel syndrome?
-sensory loss/parasthesia over palmar & distal dorsal aspects of the lateral 3 1/2 digits
-weakness/clumsiness using the hand
-weakness of thumb abduction
-thenar eminence wasting
-hand pain: typically worse at night
149
What are the special tests for carpal tunnel syndrome?
-Phalen's test: hyperflexing hands & holding dorsal surfaces together for 1 minute reproduces symptoms
-Tinel test: percussion over median nerve proximal to the carpal tunnel reproduces symptoms
150
What is the path of the ulnar nerve?
-originates from brachial plexus
-medial to brachial artery in the upper arm
-passes between medial epicondyle & olecranon
-runs through the cubital tunnel (at the elbow) and Guyon's canal (at the wrist)
151
What is the sensory function of the ulnar nerve?
-little finger & medial side of ring finger
-medial side of the dorsum of the hand
152
What is the motor function of the ulnar nerve?
-in the forearm: flexor carpi ulnaris, flexor digitorum profundus
-intrinsic muscles of the hand & hypothenar muscles
153
What are possible causes of cubital tunnel syndrome?
-trauma (e.g. distal humerus fracture)
-prolonged elbow flexion
-leaning on the elbow
-osteophyte formation due to arthritis
-mass lesions
154
What are the clinical features of ulnar nerve neuropathy?
-sensory loss/parasthesia over little finger and ring finger
-grip weakness
-wasting of the hypothenar eminence/interossei muscles
-claw hand deformity in severe cases
155
What is the path of the radial nerve?
-branches off the brachial plexus
-runs along the radial groove of the humerus
-wraps around humerus & passes anteriorly to the lateral epicondyle & through the cubital fossa
-gives off superficial sensory branch & deep motor branch
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What is the sensory function of the radial nerve?
sensory innervation to the dorsal aspect of the radial 3 1/2 digits
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What is the motor function of the radial nerve?
-triceps
-extensor muscles of the forearm
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What are the typical causes of radial nerve palsy?
-mid-humeral fracture
-Saturday night palsy (arm placed over chair etc for an extended period)
-posterior interosseous syndrome (due to compression of the posterior interosseous branch)
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What are the clinical features of radial nerve palsy?
-wrist drop
-weakness of finger extension
-sensory loss/parasthesia over dorsum of hand
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What is the path of the common peroneal nerve?
-terminal branch of the sciatic nerve (L4-S2)
-also known as common fibular
-passes through the popliteal fossa, then around the head of the fibula
-divides into superficial & deep peroneal nerves
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What are the functions of the superficial peroneal nerve?
-sensory: skin over anterolateral skin & top of foot
-motor: muscles in lateral compartment of lower leg
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What are the functions of the deep peroneal nerve?
-sensory: space between big toes & 2nd toe
-motor: muscles in the anterior compartment of the lower leg
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What are the possible causes of peroneal nerve palsy?
-trauma/injury to the knee
-external compression from tight splint, leg crossing etc.
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What are the clinical features of peroneal neuropathy?
-foot drop
-tripping over when walking
-sensory loss over the dorsum of foot & lateral shin
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What are the diagnostic tests for mononeuropathies?
-electrodiagnostic tests (EMG, NCS) to confirm the neuropathy
-imaging to identify the cause of the compression
-specific blood tests depending on the suspected cause (e.g. thyroid function & DM in carpal tunnel)
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What is multiple sclerosis?
-chronic, immune-mediated demyelinating neuroinflammatory condition
-demyelination can lead to scarring & secondary neuronal loss
-usually has relapsing-remitting course
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What is the mean age of onset of MS?
20-40 years
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What are the causes/risk factors for developing MS?
-genetic predisposition
-viral infections (EBV/glandular fever)
-low sunlight exposure & vitamin D
-others: obesity, smoking, female
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What is the pathophysiology of MS?
-destruction of oligodendrocytes (which are important in myelin sheath formation)
-possible autoimmune cause
-formation of MS plaques
-inflammation, scarring, axonal injury
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Which sites in the brain are typically affected in MS?
-optic nerves
-spinal cord
-brainstem (may present with ophthalmoplegia)
-cerebellum (ataxia & gait disturbance)
-juxtacortical white matter
-periventricular white matter
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What are the classifications of MS?
-relapsing-remitting (85-90%): episodes of exacerbation followed by periods of recovery
-primary progressive (10-15%): sustained progression of severity from onset of disease
-secondary progressive: disease course switches from relapsing-remitting to progressive
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What are the visual manifestations of MS?
-optic neuritis: visual loss, pain, scotoma, poor colour differentiation, RAPF, optic nerve swelling
-eye movement disorders: intranuclear ophthalmoplegia (INO) & abducens palsy
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What are the motor manifestations of MS?
-weakness & ataxia
-UMN signs: spasticity, reduced power, hyper-reflexia)
-transverse myelitis: inflammation in the SC causing parasthesia & weakness below the level
-cerebellar syndrome: ataxia, slurred speech, tremor, nystagmus, vertigo, clumsiness
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What are the sensory/autonomic manifestations of MS?
-parasthesia
-pain
-heat sensitivity
-sexual dysfunction
-bladder & bowel dysfunction
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What are the cognitive.psychological manifestations of MS?
-cognitive impairment (memory, attention, concentration)
-fatigue
-depression
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How is a diagnosis of MS made?
-clinical diagnosis, supported by the use of MRI
-based on MS attack supported by objective clinical evidence (e.g. MRI)
-McDonald criteria
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What are oligoclonal bands?
-bands of immunoglobulins found in the CSF of 95% of patients with MS
-can be used as markers of dissemination
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What are the general principles of management of MS?
-bladder dysfunction: anticholinergics, botox injections, self-catheterisation
-bowel dysfunction: dietary changes, laxatives, enemas
-depression: SSRIs
-fatigue: non-pharmacological interventions, modafinil (CNS stimulant)
-pain: amitriptyline, gabapentin, pregabalin
-spasticity: physiotherapy, baclofen (muscle relaxant), botox injections
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What is the management of an acute relapse of MS?
-steroids: oral or IV
-gastroprotection: PPI
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What factors are linked to prognosis in MS?
-disease type: relapsing-remitting has better prognosis than primary progressive
-incomplete recovery after first attack = worse prognosis
-clinical manifestations at onset: pyramidal, brainstem, and cerebellar symptoms (poor prognosis). Sensory symptoms, optic neuritis (favourable prognosis)
-pregnancy: protective during pregnancy. Increased risk of relapse in postpartum period.
-imaging: lesion load and cerebral atrophy linked to prognosis (higher burden and increased atrophy have worse prognosis)
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What is myasthenia gravis?
-autoimmune disorder
-formation of antibodies by B lymphocytes that bind to the ACh receptors at the NMJ
-this prevents binding of ACh, leading to increasing muscle weakness with repeated use
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What are the peak age incidences of myasthenia gravis?
20-30 years (most females) and 60-70 years (mostly males)
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What is the link between myasthenia gravis and the thymus gland?
-thymus gland is involved in +ve and -ve selection of T lymphocytes
-10-15% of patients with MG have a thymoma (benign thymus gland tumour)
-85% have thymic hyperplasia
-disease may improve with removal of the thymus gland
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What is the pathophysiology of myasthenia gravis?
-AChR-Abs bind to ACh-R on skeletal muscle (type II hypersensitivity reaction)
this has several effects on the NMJ:
-blocks ACh binding
-causes cross-linking and destruction of ACh-R
-complement-mediated destruction of the post-synaptic membrane
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How are the different subtypes of myasthenia gravis classified?
-clinical subtypes: ocular, generalised
-antibody subtypes: ACh-R, anti-MuSK, anti-LRP4, seronegative
-thymic abnormalities: normal, thymoma, hyperplasia, atrophy
-age of onset: neonatal, juvenile, early-onset (<50), late-onset
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What are the clinical features of ocular myasthenia gravis?
-diplopia
-ptosis
-weak eye movements
-pupillary sparing
-symptoms worse at the end of the day
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What are the clinical features of generalised myasthenia gravis?
-bulbar symptoms: fatiguable chewing, dysarthria, dysphagia
-weakness of facial muscles
-weakness of neck muscles
-proximal muscle weakness, arms more affected than legs
-weakness of respiratory muscles
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What is the ice pack test in myasthenia gravis?
ptosis improves are application of ice to the eyelid for 1 minute (neuromuscular transmission is better at lower temp)
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How is a diagnosis of myasthenia gravis made?
-based on clinical features and serological testing
-ice pack test, serum antibodies, electromyography (EMG), CT/MRI of thymus gland
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What is the management of myasthenia gravis?
-acetylchoniesterase inhibitors (pyridostigmine)
-corticosteroids (prednisolone)
-immunosuppressants (azathioprine)
-thymectomy
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What is myasthenic crisis?
-life-threatening condition
-worsening of weakness that requires respiratory support
-requires ITU admission
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What is the management of myasthenic crisis?
-FVC to monitor respiratory function
-IV immunoglobulines
-plasma exchange
-corticosteroids
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What are the precipitating factors of myasthenic crisis?
-warm weather
-surgery
-stress
-infections/illness
-co-morbidities
-pregnancy
-medications: Abx, antihypertensives, anti-arrhythmics etc.
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What are the primary features of Parkinsonism?
-bradykinesia
-resting tremor
-rigidity
-postural instability
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What is the peak age of onset of Parkinson's disease?
55-65 years
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What is the pathophysiology of Parkinson's disease?
-loss of 50-80% of neurones within the substantia nigra
-this affects the modulation of pyramidal motor output, causing problems with initiating movement
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What are some of the associated symptoms of Parkinson's disease?
-expressionless face
-small writing
-soft voice
-drooling
-shuffling gait
-positive Glabellar tap
-depression
-bowel & bladder symptoms
-sleep disorder
-sexual dysfunction
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How is Parkinson's disease diagnosed?
-identification of features of Parkinsonian syndrome
-exclusion of differential diagnoses (e.g. stroke, trauma, tumour, hydrocephalus, negative response to levodopa etc.)
-identification of supportive features of Parkinson's disease
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What are the investigations for Parkinson's disease?
-neuroimaging (CT/MRI)
-PET scanning with fluorodopa
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What are the pharmacological management options for Parkinson's disease?
-levodopa (given in combination with DOPA decarboxylase inhibitor)
-dopamine agonists
-MAO-B inhibitors
-COMT inhibitors
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What are the different types of peripheral neuropathies?
-radiculopathies (involves spinal nerve root)
-polyneuropathies (dysfunction of multiple nerves in the PNS)
-mononeuropathies (dysfunction of a single peripheral nerve)
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What are the commonest causes of peripheral neuropathies?
-diabetes mellitus
-carcinomatous neuropathy
-B vitamin deficiency (B12/thiamine/folate)
-drugs (Abx, amiodarone, statins, hydralazine, phenytoin)
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What are the different mechanisms of peripheral nerve damage?
-axonal degeneration
-Wallerian degeneration (compression or lesion)
-demyelination
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What is the typical distribution of polyneuropathies?
'glove and stocking' distribution, as more distal nerves are affected first
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What is the typical distribution of radiculopathies?
dermatomal/myotomal, as radiculopathies affect spinal nerve roots
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What is mononeuritis multiplex?
simultaneous peripheral neuropathy of 2+ separate nerves (e.g. common peroneal neuropathy + ulnar neuropathy)
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What are the investigations for peripheral neuropathy?
-electromyography (evaluates muscle units)
-nerve conduction studies (evaluates peripheral nerves)
-investigations to determine the cause (FBC, TF, autoimmune tests, serology, imaging)
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What is the management of peripheral neuropathy?
-treatment of underlying cause
-neuropathic analgesia (gabapentin, duloxetine)
