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Neuroscience Flashcards

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1
Q

What is migraine?

A

Severe, episodic headache that may have a prodrome of focal neurological symptoms (aura) and is associated with systemic disturbance

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2
Q

Recall the medical management of migraine both in the acute setting and for prophylaxis

A

Acute:

  1. Anti-emetic - IV metoclopramide
  2. Analgesia - aspirin, paracetamol, NSAID (NO OPIOIDS)
  3. Triptan (5HT1-R agonist) - sumitriptan

Prophylaxis:
1st line = propranolol (BB) or topiramirate (anticonvulsant)
2nd line = TCA - amitriptyline

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3
Q

When does migraine usually present?

A

Teenager - young adult OR middle age

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4
Q

What are the risk factors for migraine?

A

FHx
Lifestyle - caffeine, stress, lack of sleep
Change in barometric pressure - high altitude/weather changes
Female
Obesity - increases risk of chronic migraine
Habitual snoring
Overuse of headache meds

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5
Q

What are the symptoms of migraine?

A 
Prolonged headache - 4-72h
Episodic/recurrent
Throbbing/pulsating
N+V
Decreased ability to function
Headache worse with activity
Sensitivity to light/smell/noise
Aura
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6
Q

What causes migraine?

A

Brain is hyperexcitable to a variety of stimuli

Neuronal depolarisation is more easily triggered

Genetic

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7
Q

How is migraine diagnosed?

A

Clinically

Any investigations are normal

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8
Q

What are the complications of migraine?

A

Status migrainosus - migraine attack > 72h - ?medication overuse as cause, tx w corticosteroids

Depression
Chronic migraine
Seizures
Migrainous infarction

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9
Q

What is Bell’s palsy?

A

Acute unilateral peripheral facial nerve (CNVII) palsy

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10
Q

How is Bell’s palsy diagnosed?

A

Clinical diagnosis of exclusion

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11
Q

What are the risk factors for Bell’s palsy?

A

Intranasal flu vaccine

Pregnancy

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12
Q

What are the symptoms of Bell’s palsy?

A
  1. Single episode
  2. Unilateral
  3. No constitutional symptoms
  4. Dry eyes
  5. Post-auricular pain
  6. Otalgia
  7. Sometimes sensory disturbances
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13
Q

What are the signs of Bell’s palsy?

A

Acute, unilateral facial palsy, with an o/w normal physical examination

Equal distribution of facial weakness across facial zones

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14
Q

Why does Bell’s palsy affect the whole face?

A

Involves all nerve branches (bc blockade originates proximal to geniculate ganglion, prior to any branching)

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15
Q

What causes Bell’s palsy?

A

Reactivation of HSV-1 within the geniculate ganglion after cellular immune suppression

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16
Q

What is the most common cause of unilateral facial palsy in those over 2?

A

Bell’s palsy

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17
Q

In what age group is Bell’s palsy most common?

A

15-45yo

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18
Q

How is Bell’s palsy managed acutely?

A
  1. Corticosteroid - prednisolone - 60mg OD for 5 days, then daily down 10mg until 0 - start within 72h of onset
  2. Eye protection
    - glasses + artificial tears during day
    - ophthalmic lubricant + eyelid taped shut at night
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19
Q

What is the prognosis for Bell’s palsy?

A

Incomplete paralysis on presentation - 94% fully recover

vs 61% of those with complete paralysis

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20
Q

What is cluster headache?

A

Unilateral headache attacks lasting from 15-180 minutes associated w/autonomic symptoms (parasympathetic hyperactivity and sympathetic hypo-activity)

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21
Q

What are the risk factors for cluster headache?

A 
Male
FHx
Head injury
Smoking
Heavy drinking
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22
Q

What is the most common trigger for cluster headache?

A

Alcohol

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23
Q

What are the signs and symptoms of cluster headache?

A 
Unilateral headache attack
15m-3h
Around 4/day
Excruciating pain
Autonomic: lacrimation, rhinorrhoea, partial Horner's
Agitated - can't sit still
Photophobia + phonophobia
Migrainous aura
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24
Q

Recall the aetiology of cluster headache

A

Idiopathic

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25
How is cluster headache investigated?
Brain CT/MRI - normal in primary, abnormal in secondary (tumour, cavernous sinus pathology) ESR - normal in primary, to exclude GCA in patients > 50 Pituitary function tests - normal, abnormalities --> secondary causes resulting from pituitary adenoma
26
What is encephalitis?
Inflammation of the brain parenchyma associated with neurological dysfunction
27
Recall the aetiology of encephalitis
Mainly viral | Usually HSV-1
28
What are the risk factors for encephalitis?
``` Age <1 or >65 Immunodeficiency Viral infections Blood/body fluid exposure Organ transplant Animal or insect bites Swimming or diving in warm freshwater or nasal/sinus irrigation ```
29
What are the presenting symptoms of encephalitis?
``` Fever Rash Altered mental state - drowsy-coma Headache Photophobia Neck stiffness Seizure ```
30
What are the signs of encephalitis?
``` Pyrexia Altered mental state Focal neurological deficit Meningismus - headache, photophobia, neck stiffness Seizures ```
31
How is encephalitis investigated?
``` 1. BLOODS FBC - high lymphocytes UE - SIADH possible (low Na) Glucose - compare w CSF glucose Viral serology ABG ``` 2. MRI/CT --> HSV - temporal oedema Also exclude mass lesion before LP 3. LP: high lymphocytes and monocytes + high protein Culture/PCR
32
Why must you do a CT brain before a lumbar puncture in suspected encephalitis?
To exclude a mass lesion
33
What is extradural haemorrhage?
Bleeding between the dura mater and the inner surface of the skull
34
What is subdural haemorrhage?
Bleeding into the subdural space (between dura and arachnoid mater)
35
What is subarachnoid haemorrhage?
Bleeding into the subarachnoid space (between arachnoid and pia mater)
36
What causes subdural haemorrhage?
Usually TRAUMA: Blow to temporal side of head Ruptures bridging cranial veins ``` Also: Rupture of cerebral aneurysm Rupture of arteriovenous malformation Cerebral hypotension Malignancy (rare) ```
37
What causes subarachnoid haemorrhage?
Traumatic injury OR spontaneous ``` Spontaneous causes: Ruptured intracranial aneurysms 70% Arteriovenous malformation 10% Unknown aetiology 15% Rare disorders <5% ```
38
What is the classic history for extradural haemorrhage?
Head trauma + severe headache Immediate fluctuating level of consciousness following trauma before appearing lucid (lucid interval) - tiredness, confusion Rapid deterioration some time following regaining consciousness
39
What are the earl signs of extradural haemorrhage?
Severe headache after trauma, can persist Initial loss/fluctuance in consciousness - tiredness, confusion Period of lucidity after initial LOC - lasts 6-8h, but can last days
40
What investigations must be done for extradural haemorrhage?
Urgent non-contrast CT head
41
What does an extradural haemorrhage look like on CT?
Lemon Biconvex lens Midline shift Brain stem herniation
42
What are the late signs of extradural haemorrhage
1. GCS drops as ICP rises and BS begins to herniate 2. LOC 3. Focal neurological deficitis in eyes (CN compression) - blown pupil = fixed dilated ipsilateral pupil 4. Contralateral hemiparesis, can become bilateral (compression of ipsilateral motor cortex) 5. UMN signs - positive Babinski's sign (upgoing toes), hyperreflexia + hypertonia 6. Cushing's triad due to raised ICP 7. Persisting unconsciousness -deep coma and v low GCS 8. Death - resp arrest
43
What upper motor neuron signs may you see in EDH?
Positive Babinski's - upgoing toes Hyperreflexia Hypertonia - spasticity
44
What is Cushing's triad and what causes it?
Bradycardia HTN Deep/irregular breathing Raised ICP
45
What investigation are absolutely contraindicated in EDH and why?
Lumbar puncture Result in drop in CSF pressure May speed up brain herniation
46
What investigation are absolutely contraindicated in EDH and why?
Lumbar puncture Result in drop in CSF pressure May speed up brain herniation
47
What are the risk factors for subdural haemorrhage?
Recent trauma Coagulopathy Anticoagulant use >65yo
48
What are the presenting symptoms of SDH?
``` Headache N+V Confusion Irritability Seizure ```
49
What are the signs of SDH?
Head trauma - abrasions, lacerations Low GCS: Diminished eye response: anisocoria (unequal pupil size) - BS herniation Diminished verbal response Diminished motor response Confusion Focal neurological signs (much more common in acute)
50
How is SDH investigated?
Urgent non-contrast CT: banana/moon
51
How is SDH managed initially?
Resuscitation and stabilisation of vitals: ABCDE | Senior doctor + neurosurgeon + anaesthetist
52
What are the complications of SDH
Complications result from damage from bleed itself + standard post-op complications from surgical Mx ``` Neuro deficits Coma Seizure Infection Recurrent haemorrhage ```
53
What are poorer functional outcomes in SDH associated with?
``` Older age More serious injury Lower GCS Midline shift, multiple parenchymal lesions Raised ICP Early need for surgery ```
54
How can SDH be classified?
Acute <3d | Chronic >21d
55
How does SDH clinically present?
``` History of trauma Older Alcohol misuse Child - non-accidental injury Gradual deterioration (worsening headache and confusion) ```
56
How is acute SDH managed once confirmed by non-contrast CT?
Bleed <10mm size (midline shift <5mm non-expansile without significant neurological dysfunction): 1. Admit, observe, monitor + follow-up CT in 2-3wks 2. Prophylactic antiepileptics - IV phenytoin, phenobarbital or oral/IV levetiracetam 3. ICP monitoring if GCS is <9 4. Correct coagulopathies (i.e. vitamin K) 5. Lower ICP Bleed w 1+ of following: ≥10mm size; w midline shift >5mm; expansile or significant neurological dysfunction - SURGERY FIRST - decompressive craniectomy
57
What does the management of acute SDH once confirmed depend on?
Size of haemorrhage
58
How is chronic SDH managed once confirmed?
1. Antiepileptic medication - IV phenytoin, IV phenobarbital, oral/IV levetiracetam 2. Surgery for symptomatic patients- i.e. burr hole irrigation and drainage, craniotomy 3. Correct coagulopathy- i.e. with vitamin K 4. Lower ICP
59
What are the 3 main ways in which SAH damages the brain?
1. Hypoxia 2. Raised ICP 3. Direct cranial injury
60
What are the risk factors for spontaneous SAH?
``` HTN Smoking FHx Autosomal dominant polycystic kidney disease <50yo Female (1.5x baseline risk) Black ```
61
Compare the pathophysiology of EDH, SDH and SAH
EDH: rupture of middle meningeal artery on temporal surface of skull SDH: rupture of bridging cranial veins SAH: rupture of a berry aneurysm
62
How does SAH clinically present?
Sudden onset severe headache, reaching max intensity within seconds = thunderclap headache N+V Photophobia Reduced consciousness level Neck stiffness Kernig's sign
63
What is Kernig's sign?
Patient is supine w hip and knee flexed to 90 degrees Inability/pain on straightening leg
64
What causes a positive Kernig's sign?
Irritation of motor nerve roots passing through inflamed meninges as they are under tension
65
How is SAH investigated?
Bloods: FBC, U+Es, coagulation studies (useful prior to LP or surgery) Urgent plain CT head - blood in SA space or hydrocephalus CT angiogram - can identify aneurysm LP - only if SAH suspected but CT clear and no evidence of raised ICP
66
When is a lumbar puncture necessary in suspected SAH?
When CT scan clear and shows no evidence of raised ICP (risk of BS coning)
67
When must a lumbar puncture be performed in suspected SAH for the results to be reliable?
At least 12h after onset of symptoms
68
What does an LP show in SAH?
Xanthochromia Due to infiltration of blood from haemorrhage Bilirubin Oxyhaemoglobin
69
What is Guillain-Barré syndrome?
Acute inflammatory demyelinating polyneuropathy
70
Recall the aetiology of GBS
- Immune-mediated demyelination of PNS | - Often triggered by Campylobacter infection (or Salmonella) about 2 weeks after infection
71
What are the risk factors for GBS?
Preceding viral illness - gastroenteritis or flu-like weeks before onset Preceding bacterial infection Hep E infection Increasing age
72
What are the presenting symptoms of GBS?
- Ascending symmetrical muscle weakness/paralysis a few weeks after infection - Proximal muscles more affected - trunk, resp, CN VII esp - Pain - back, limb - Autonomic: sweating, high HR, BP changes, arrhythmia, urinary retention - Areflexia - Diplopia - Slurred speech
73
What are the signs of GBS?
- Symmetrical muscle weakness/paralysis - Proximal muscles - Tachycardia - Areflexia
74
How is GBS investigated?
1. ABs: 25% +ve for anti-GM1 2. NCS: slow conduction 3. LP - CSF: high protein <5.5g/L; normal WCC 4. Spirometry to monitor lung function (diaphragm involvement)
75
What are anti-GM1 antibodies indicative of?
Guillain-Barre syndrome
76
What symptoms make up Horner's syndrome?
Ptosis Miosis Anhydrosis
77
What causes Horner's syndrome?
Disruption of SNS to face | Lesion
78
Where is the lesion located in Horner's syndrome?
Ipsilateral side of symptoms
79
What tests are used in Horner's syndrome?
Cocaine eye drops - should block reuptake of post-ganglionic NA --> lack of NA in cleft --> mydriatic failure (no effect) Paredrine - helps localise cause - if 3rd order neuron intact, amphetamine causes NT vesicle release --> NA into cleft --> mydriasis - if lesion in of 3rd order neuron - no effect - pupil stays constricted Dilation lag test
80
How is Horner's syndrome managed?
Depends on location and cause of lesion of tumour Surgical removal Radiation and chemotherapy Genetic counselling if have genetic form
81
What is Huntington's disease?
An autosomal dominant, slowly progressive, neurodegenerative disorder
82
When does Huntington's disease usually appear?
Mid-adult life
83
Recall the aetiology of Huntington's disease
Caused by an expanded CAG repeat at the N-terminus of the gene that codes for the huntingtin protein
84
What are the symptoms of Huntington's disease?
``` Chorea Personality change Irritability and impulsivity Twitching or restlessness Loss of coordination Deficit in fine motor coordination Slowed saccades Motor impersistence Impaired tandem walking ```
85
What are the signs of Huntington's disease?
Slowed saccades - ask pt to look between your 2 fingers held shoulder width apart - head turning or eye blinking Motor impersistence - ask pt to protrude tongue or close eyes tightly for 10s - pt struggles to maintain Deficit in fine motor coordination - tapping finger to thumb quickly - pt slow and irregular tempo
86
How is Huntington's disease investigated?
Nothing initially - clinical diagnosis CAG repeat testing can be done later - 40+ CAG repeats on 1 of the 2 alleles = +ve intermediate result = 36-39 repeats MRI/CT - evident caudate or striatal atrophy
87
What eye sign is present in Huntington's disease?
Slowed rapid (saccadic) eye movements
88
What eye sign is present in Huntington's disease?
Slowed rapid (saccadic) eye movements
89
What is hydrocephalus?
Excessive accumulation of CSF within the brain
90
What causes hydrocephalus?
``` Congenital (birth defects): Aqueductal stenosis Neural-tube defects Arachnoid cysts Dandy-Walker syndrome Arnold-Chiari malformation ``` ``` Acquired: CNS infections Meningitis Brain tumours Head trauma Toxoplasmosis SAH or intraparenchymal haemorrhage ```
91
What are the 3 types of hydrocephalus?
1. Non-communicating/obstructive - impaired CSF flow 2. Communicating/non-obstructive - impaired reabsorption 3. Excessive CSF production
92
What are the signs and symptoms of hydrocephalus?
Varies with chronicity Acute dilatation of ventricular system manifests w non-specific S&Ss of raised ICP: - Headaches worse in morning - Get better sitting upright but eventually become continuous - N+V - Papilloedema - Sleepiness or coma Chronic dilatation (esp in elderly): insidious onset w Hakim's triad: 1. Gait instability 2. Urinary incontinence 3. Dementia
93
What is lumbar puncture?
A needle is inserted into the spinal canal, most commonly to collect CSF for diagnostic testing
94
What are the indications for an LP?
1. Diagnose CNS diseases eg meningitis, SAH 2. Inject meds - analgesia, ABx, chemo 3. Spinal anaesthetic (epidural) 4. Remove some fluid to reduce pressure in skull or spine
95
What are the possible complications of an LP?
Post spinal headache w nausea Parasthesia in leg during procedure Spinal/epidural bleeding Adhesive arachnoiditis SC trauma
96
What is meningitis?
An acute inflammation of the meninges
97
Recall the aetiology of meningitis
``` Viral/bacterial/fungal/protozoal infection Drugs - NSAIDs, ABx, IV Igs Metastasis Sarcoidosis SLE Vasculitis ```
98
What are the presenting symptoms of meningitis?
``` Headache N+V Photophobia Neck stiffness Fever Rash ```
99
How is meningitis investigated?
LP to get CSF sample Acute bacterial = low glu, high prot, PMNs Acute viral = norm glu, norm/high prot, mononuclear cells Tuberculous - low glu, high prot, mononuclear and PMNs Fungal = low glu, high prot Malignant = low glu, high prot, mononuclear cells Bloods - CRP, FBC, cultures
100
How is meningitis managed?
Bacterial: - empirical cephalosporin eg cefotaxime - corticosteroids eg dexamethasone Viral: supportive or aciclovir Fungal: long course high-dose antifungals eg amphotericin B
101
What are the possible complications of meningitis?
Deafness Epilepsy Hydrocephalus Cognitive deficits
102
What is the most common cause of meningitis?
Viral infection | HSV-1
103
What is the prognosis of meningitis?
Untreated, bacterial is almost always fatal Viral - tends to resolve spontaneously and is rarely fatal
104
What are the risk factors for meningitis?
``` Infants and young children - enteroviral Young adults - HSV-1 Older people - HSV-1 Summer and autumn in temperate regions Exposure to mosquito or tick vector - arboviruses Unvaccinated for mumps ```
105
What are the risk factors for meningitis?
``` Infants and young children - enteroviral Young adults - HSV-1 Older people - HSV-1 Summer and autumn in temperate regions Exposure to mosquito or tick vector - arboviruses Unvaccinated for mumps ```
106
What is motor neurone disease?
A group of neurodegenerative disorders that selectively affect motor neurons
107
What are the 6 types of MND?
1. Amyotrophic lateral sclerosis (ALS) 2. Progressive bulbar palsy (PBP) 3. Pseudobulbar palsy 4. Progressive muscular atrophy (PMA) 5. Primary lateral sclerosis (PLS) 6. Monomelic amyotrophy (MMA)
108
What are the symptoms of MND?
Come on slowly Worsen over course of more than 3 months Muscle cramps Spasms Exertional dyspnoea Orthopnoea Bulbar symptoms: dysarthria, dysphagia, sialorrhoea Emotional disturbance + cognitive + behavioural changes
109
What are the signs of MND?
LMN findings - muscle wasting, fasciculations, hyporeflexia | UMN findings - hyperreflexia, hypertonia, Babinski's
110
How is MND investigated?
CSF tests - infection or inflammaton MRI - other cause of UMN signs EMG + NCS - LMN signs - EMG - acute + chronic denervation and reinnervation of muscle NCS - normal Tissue biopsy (rarely)
111
What would sensation testing in MND show?
Normal | Sensation not typically affected
112
What is multiple sclerosis?
An inflammatory demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of the central nervous system (brain, spinal cord, and optic nerves) separated in time and space
113
Recall the aetiology of MS
Inflammatory and degenerative components that may be triggered by environmental factors in genetically-susceptible individuals Environmental factors - toxins, viral exposures, sunlight exposures (and its effect on vit D metabolism)
114
What are the risk factors for MS?
FHx Female Northern hemisphere
115
What are the presenting symptoms of MS?
- Graying/blurring of vision in one eye - Pain moving one eye - Loss of colour discrimination, esp reds - Odd sensations of wet patch/burning/hemibody sensory loss/tingling - Gradual onset of muscle weakness that resolves w rest - Leg cramping esp PM/driving - Fatigue - Urinary freq - Constipation - Imbalance/incoordination
116
What are the signs of MS?
- Spasticity/increased muscle tone - Increased deep tendon reflexes, asymmetrical (esp clonus at ankles) - Wide-based gait - Limb ataxia - Foot dragging - Lhermitte's sign - electric shock-like sensations extending down cervical spine radiating to limbs
117
How is MS investigated?
1. MRI brain w contrast - hyperintensities in periventricular white matter 2. MRI SC - demyelinating lesions 3. FBC - normal 4. Metabolic panel - normal 5. TSH - normal 6. Vitamin B12 - normal
118
When does MS usually present?
20-40yo
119
Describe a tension headache
Generalised location - mostly frontal and occipital regions Bilateral Non-pulsatile/dull Episodic or chronic Rarely disabling or associated w any autonomic phenomena 'Tight band' around head
120
What are the risk factors for tension headache?
Mental tension Stress Missing meals Fatigue
121
What are the signs of tension headache
Normal neuro exam | Pericranial/SCM/trapezius/temporalis/lateral pterygoid/masseter tenderness
122
How is tension headache managed?
Acute - analgesics ``` Chronic symptoms (>7-9 headache days/month): Antidepressants - amitriptyline/doxepin ```
123
What are the complications of tension headache?
Peptic ulcer due to chronic NSAID use
124
What is trigeminal neuralgia?
A facial pain syndrome in the distribution of >=1 divisions of the trigeminal nerve
125
Recall the aetiology of trigeminal neuralgia
Trigeminal nerve root compression at root entry zone by an aberrant vascular loop (usually superior cerebellar artery) Demyelinating disease - MS Other BS lesions
126
What are the risk factors for trigeminal neuralgia?
Increased age | MS
127
What are the presenting symptoms of trigeminal neuralgia?
Sharp, stabbing, intense pain lasting up to 2m + constant facial pain Without associated neurological deficit
128
What are the signs of trigeminal neuralgia?
Normal neuro exam
129
How is trigeminal neuralgia investigated?
Clinical diagnosis Intra-oral XR - ?dental cause MRI - visualise abnormal vessel loop compressing nerve/tumour/infarct/MS plaque
130
What is Wernicke's encephalopathy?
Neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations, typically involving mental status changes and gait and oculomotor dysfunction
131
What are the risk factors for Wernicke's encephalopathy?
``` Alcohol dependence AIDS Cancer and chemo Malnutrition Hx of GI surgery ```
132
Recall the aetiology of Wernicke's encephalopathy
Acute or sub-acute thiamine deficiency As a result of decreased intake, relative deficiency due to increased demand, or malabsorption from GI tract
133
What is the triad in Wernicke's?
Ataxia Ophthalmoplegia Confusion Only 10% present this way
134
How is Wernicke's encephalopathy investigated?
1. Therapeutic trial of parenteral thiamine - gets better quickly 2. Finger-prick glucose - normal 3. Bloods Normal = FBC, electrolytes, renal function, ammonia Elevated = LFTs, alcohol Low = thiamine, Mg
135
What are the presenting symptoms of Wernicke's encephalopathy?
Mental slowing, impaired concentration, and apathy Frank confusion Ocular motor findings - gaze palsies, abducens palsies, impaired vestibulo-ocular reflexes
136
What are the causes of raised ICP?
Mass effect: brain tumour, infarction w oedema, contusions, SDH, EDH, abscesses - deform adjacent brain Generalised brain swelling: ischaemic-anoxia states, acute liver failure, hypertensive encephalopathy, hypercapnia, Reye hepatocerebral syndrome - decrease cerebral perfusion pressure w minimal tissue shifts Increased venous pressure: venous sinus thrombosis, HF, obstruction of superior mediastinal/jugular veins CSF obstruction/overproduction: hydrocephlus, extensive meningeal disease/meningitis, SAH, choroid plexus tumour Idiopathic intracranial hypertension Craniosynostosis
137
What are the presenting symptoms of raised ICP?
``` Headache (morning/wake pt up from sleep/worse on coughing, sneezing, bending/progressively worsening) Vomiting without nausea Drowsy/unconscious Back pain Visual disturbances Personality/behavioural changes ```
138
What are the signs of raised ICP?
``` Ocular palsies Altered level of consciousness Papilloedema Pupillary dilatation Cushing's triad - increased SBP, bradycardia, irregular breathing ```
139
What is myasthenia gravis?
a chronic autoimmune disorder of the post-synaptic membrane at the neuromuscular junction (NMJ) in skeletal muscle
140
What are the risk factors for myasthenia gravis?
FHx of AI disorders Genetic markers - specific HLA genes and single nucleotide polymorphisms in immune system Cancer-targeted therapy: checkpoint inhibitors
141
What are the presenting symptoms of myasthenia gravis?
Muscle fatiguability - worse w activity and improves on rest Better in morning than evening Diplopia Dysphagia Dysarthria Proximal limb weakness - difficulty getting out of chair/climbing stairs
142
What are the signs of myasthenia gravis?
Ptosis Facial paresis - flat smile Proximal limb weakness
143
Recall the aetiology of myasthenia gravis
Antibodies against nAChR on post-synaptic muscle membrane at NMJ Rarely antibodies agaginst muscle-specific tyrosine kinase (MuSK) at NMJ Certain genotypes (HLA) more susceptible to making these antibodies
144
How is myasthenia gravis investigated?
1. Serum AChR antibody analysis 2. MuSK antibodies 3. Serial lung function tests (if SOB) - low FVC and NIF
145
How is raised ICP investigated?
?
146
What is neurofibromatosis?
An autosomal dominant genetic disorder affecting cells of neural crest origin, resulting in the development of multiple neurocutaneous tumours
147
Recall the aetiology of neurofibromatosis
Autosomal dominant Affects cells of neural crest origin Associated w multiple mutations in TSGs NF1 (type 1) and NF2 (type 2)
148
How many seizures must you have had in order for epilepsy to be diagnosed?
2
149
What are the presenting symptoms of neurofibromatosis?
``` Type 1: Skin lesions Learning difficulties Headaches Disturbed vision (optic gliomas) Precocious puberty (pit gland lesions) ``` ``` Type 2: Hearing loss Tinnitus Balance problems Headache Facial pain + numbness ```
150
What are the signs of neurofibromatosis?
Type 1: 5+ café au lait macules of >5mm (pre-pubertal) 5+ café au lait macules of >15mm (post-pubertal) Neurofibromas - cutaneous nodules or complex plexiform neuromas Freckling in armpit or groin Lisch nodules (hamartomas on iris) Spinal scoliosis Type 2: Few or no skin lesions Sensorineural deafness w facial nerve palsy or cerebellar signs
151
How is neurofibromatosis investigated?
1. MRI/CT/PET - tumours 2. Biopsy 3. Genetic testing 4. Ophthalmological assessment 5 . Audiometry 6. Skull XR (sphenoid dysplasia in NF1)
152
What is a generalised seizure?
Seizure that affects whole of the brain + consciousness
153
What are the 5 types of generalised seizure?
``` Tonic-clonic Absence Myoclonic Atonic Tonic ```
154
Recall the aetiology of epilepsy
Most cases are IDIOPATHIC Primary epilepsy syndromes - eg idiopathic generalised epilepsy ``` Secondary seizures: Tumour Infection Inflammation Toxic/metabolic - eg Na imbalance Drugs - alcohol withdrawal Vascular - haemorrhage Congenital abnormalities - cortical dysplasia Neurodegenerative disease - Alzheimer's Malignant HTN or eclampsia Trauma ```
155
What common things look like seizures?
Syncope Migraine Non-epileptiform seizure disorder (eg dissociative disorder)
156
What should you ask when taking a history for a potential epilepsy patient?
``` Rapidity of onset Duration of episode Any alteration in consciousness? Any tongue biting or incontinence? Any rhythmic sychcronous limb jerking? Any post-ictal abnormalities eg exhaustion, confusion? DHx eg alcohol, recreational drugs ```
157
What are the symptoms of a tonic-clonic seizure?
Vague symptoms before attack - irritability Tonic phase - generalised muscle spasm Clonic phase - repetitive synchronous jerk Faecal/urinary incontinence Tongue biting Post-ictal phase: impaired consciousness, lethargy, confusion, headache, back pain, stiffness
158
What are the symptoms of an absence seizure?
Onset in childhood Loss of consciousness but maintained posture Stops talking and stares into space for few seconds NO post-ictal phase
159
What are the symptoms of a frontal lobe focal motor seizure?
Motor convulsions Jacksonian march - muscular spasm caused by simple partial seizure spreads from affecting distal part of limb towards ipsilateral facce Post-ictal flaccid weakness (Todd's paralysis)
160
What are the symptoms of a temporal lobe seizure?
Aura - visceral or psychic symptoms | Hallucinations - olfactory or affecting taste
161
What are the symptoms of a frontal lobe complex partial seizure?
LOC Involuntary actions/disinhibition Rapid recovery
162
Describe non-convulsive status epilepticus
Acute confusional state Often fluctuating Difficult to distinguish from dementia
163
How is epilepsy investigated?
Bloods - FBC, U+E, LFTs, glu, Ca, Mg, ABG, toxicology, prolactin (post-ictal increase) EEG - helps confirm diagnosis, classify epilepsy CT/MRI - structural, space-occupying or vascular lesions
164
What are the possible complications of epilepsy?
1. Fractures from tonic-clonic seizures 2. Behavioural problems 3. Sudden death in epilepsy (SUDEP)
165
What are the complications of common anti-epileptic drugs?
Phenytoin - gingival hypertrophy Carbamazepine - neutropaenia and osteoporosis Lamotrigine - Stevens-Johnson syndrome
166
Summarise the prognosis for patients with epilepsy
50% remission at 1 year
167
What is status epilepticus?
A seizure lasting > 30 mins or repeated seizure without recovery and regain of consciousness in between
168
How is status epilepticus treated?
ABC approach 1. Give glucose if hypoglycaemic 2. IV lorazepam or IV/PR diazepam 3. Repeat step 2 after 10 mins if seizure doesn't stop 4. If seizure doesn't stop - IV phenytoin + ECG monitor 5. If seizure doesn't stop, GA (thiopentone) + intubation + mech ventilation 6. TREAT CAUSE
169
How are focal seizures treated?
Lamotrigene or carbamazepine
170
How are generalised seizures treated?
Sodium valproate
171
List some anti-convulsants
``` Lamotrigene Carbamazepine Sodium valproate Phenytoin Levetiracetam Clobazam Topiramate Gabapentin Vigabatrin ```
172
What is spinal cord compression?
Injury to the spinal cord with neurological symptoms dependent on the site and extent of the injury
173
Recall the aetiology of spinal cord compression
MOST CASES: trauma and tumours (mets) Other: Spinal abscess TB (Pott's disease)
174
How can trauma lead to spinal cord compression?
1. Direct cord contusion 2. Compression by bone fragments 3. Haematoma 4. Acute disk prolapse
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What are the risk factors for spinal cord compression?
Trauma Osteoporosis Metabolic bone disease Vertebral disc disease
176
What are the presenting symptoms of spinal cord compression?
``` Hx of trauma or malignancy Pain Weakness Sensory loss Disturbance of bowel and bladder function ```
177
What are the signs of spinal cord compression?
``` Diaphragmatic breathing Reduced anal tone Hyporeflexia Priapism (persistent and painful erection) Spinal shock (low BP wo tachycardia) Sensory loss - at level of lesion Motor: - weakness/paralysis - downwards plantars in acute phase - UMN signs below lesion - LMN at level of lesion ```
178
What can a large central lumbar disc prolapse cause?
1. Bilateral sciatica 2. Saddle anaesthesia 3. Urinary retention
179
Identify appropriate investigations for spinal cord compression
Radiology: 1. Lateral radiographs of spine - look for loss of alignment, fractures, etc 2. MRI/CT Bloods: FBC, U+E, Ca, ESR, Ig electrophoresis (multiple myeloma) Urine: Bence-Jones proteins (multiple myeloma)
180
What is stroke?
Rapid permanent neurological deficit from cerebrovascular insult Clinically: Focal or global impairment of CNS function developing rapidly and lasting > 24 hours
181
Recall the aetiology of stroke
Infarction (80%): 1. Thrombosis - lacunar infarcts, in MCA 2. Emboli - carotid dissection, carotid atherosclerosis, AF 3. Hypotension 4. Others - vasculitis, cocaine (arterial spasm) Haemorrhage (10%): 1. HTN 2. Charcot-Bouchard microaneurysm rupture 3. Amyloid angiopahty 4. Arteriovenous malformations - Less common: trauma, tumours, vasculitis
182
What is a lacunar infarct?
Thrombosis in small vessels
183
How can hypotension cause stroke?
If the BP is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories Most distal capillaries vasoconstrict
184
What are the presenting symptoms of stroke?
``` Weakness Sensory, visual or cognitive impairment Impaired coordination Impaired consciousness Head or neck pain (if carotid/vertebral artery dissection) ```
185
What should you ask about in the history for ?stroke?
Time of onset (critical for emergency Mx) | Hx of AF, MI, valvular HD, carotid artery stenosis, recent neck trauma or pain
186
What are the signs of a lacunar infarct?
Affecting the internal capsule or pons: pure sensory or motor deficit or both Affecting thalamus: LOC, hemisensory deficit Affecting basal ganglia: hemichorea, hemiballismus, parkinsonism
187
What are the signs of an anterior cerebral infarct?
Lower limb weakness | Confusion
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What are the signs of a middle cerebral infarct?
Facial weakness Hemiparesis (motor cortex) Hemisensory loss (sensory cortex) Apraxia Hemineglect (parietal lobe) Receptive/expressive dysphasia (Wernicke's/Broca's areas) Quadrantopia (superior/inferior optic radiations)
189
What is the sign of a posterior cerebral infarct?
Hemianopia
190
What are the signs of an anterior inferior cerebellar infarct?
Vertigo Ipsilateral ataxia Ipsilateral deafness Ipsilateral facial weakness
191
What are the signs of a posterior inferior cerebellar infarct?
``` Vertigo Ipsilateral ataxia Ipsilateral Horner's syndrome Ipsilateral hemisensory loss Dysarthria Contralateral spinothalamic sensory loss ```
192
What are the signs of a basilar artery infarct?
CN pathology | Impaired consciousness
193
What are the signs of multiple lacunar infarcts?
``` Vascular dementia UI Gait apraxia Shuffling gait Normal or excessive arm-swing ```
194
What are the signs of an intracerebral infarct?
``` Headache Meningism Focal neurological signs N+V Signs of raised ICP Seizures ```
195
How is stroke investigated?
Bloods: clotting profile - check if thrombophilia ECG - check for arrhythmias Echocardiogram - identify cardiac thrombus, endocarditis, etc Carotid doppler US CT head - rapid detection of haemorrhages MRI brain - look for infarction CT cerebral angiogram - dissections or intracranial stenosis
196
How is stroke managed acutely?
If < 4.5h from onset: 1. Exclude haemorrhage by CT head 2. Thrombolysis - IV ALTEPLASE (tPA) 3. 300mg ASPIRIN 24h later 4. Swallowing assessment 5. Heparin + early mobilisation if high risk of emboli recurrence/stroke progression If > 4.5h from onset: 1. Exclude haemorrhage on CT head 2. ASPIRIN + CLOPIDOGREL 3. HEPARIN + early mobilisation if high risk of emboli recurrence/stroke progression
197
How is stroke prevented?
Aspirin + dipyidamole Warfarin (AF) Control RFs: HTN, hyperlipidaemia, treat carotid artery disease Surgical Tx: carotid endarterectomy
198
What are the possible complications of stroke?
``` Cerebral oedema - raised ICP Immobility Infections DVT CV events Death ```
199
Summarise the prognosis for patients with stroke
10% mortality in 1st month Up to 50% that survive are dependent on others 10% recurrence within 1 year Prognosis worse for haemorrhagic than ischaemic
200
What are the different types of neurofibromatosis?
``` Type 1: Peripheral + spinal neurofibromas Multiple café au lait spots Freckling (armpit/groin) Optic nerve glioma Lisch nodules Skeletal deformities Phaeochromocytomas Renal artery stenosis ``` ``` Type 2: Schwannomas Meningiomas Gliomas Cataracts ```
201
What is Parkinson's disease
Neurodegenerative disease of the dopaminergic neurones of the substantia nigra
202
Recall the aetiology of Parkinson's disease
Sporadic/idiopathic: Most common Aetiology unknown May be related to environmental toxins and oxidative stress Secondary: Neuroleptic therapy (eg for schizophrenia) Vascular insults (eg in basal ganglia) MPTP toxin from illicit drug contamination Post-encephalitis Repeated head injury Some familial forms of PD
203
What are the presenting symptoms of Parkinson's disease?
``` Insidious onset Resting tremor (hands) Stiffness and slowness of mvmts Difficulty initiating mvmts Frequent falls Smaller handwriting (micrographia) Insomnia Mental slowness ```
204
What are the signs of Parkinson's disease?
Asymmetrical pill-rolling resting tremor - reduced on action Lead pipe rigidity - superimposed tremor --> cogwheel rigidity Stooped, shuffling, small-stepped gait - reduced arm swing - difficulty initiating walking Postural instability - falls easily ``` Frontalis overactivation - furrowed brow Hypomimic face Soft monotonous voice Impaired olfaction Drooling Mild impairment of up-gaze Depression Cognitive problems and dementia ```
205
How is Parkinson's disease investigated?
Clinical diagnosis 1. Levodopa trial - timed walking and clinical assessment after drug 2. Bloods - serum caeruloplasmin - rule out Wilson's disease (excess copper) as cause 3. CT/MRI brain - exclude other causes of gait decline eg hydrocephalus 4. Dopamine transporter scintigraphy - reduction in striatum and putamen
206
What is a TIA?
Transient ischaemic attack Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours
207
Recall the aetiology of TIA
Usually embolic, but may be thrombotic Most common source of emboli = carotid atherosclerosis Emboli can also arise from heart: AF, mitral valve disease, atrial myxoma
208
What are the risk factors for TIA?
``` HTN Smoking DM Heart disease Peripheral arterial disease Polycythaemia rubra vera COCP Hyperlipidaemia Alcohol Clotting disorders ```
209
What are the presenting symptoms of TIA affecting the 2 most common territories?
Usually last 10-15 mins ``` Carotid: Unilateral Motor area: weakness of an arm, leg, or one side of face Dysarthria Broac's dysphasia Amaurosis fugax ``` Vertebrobasilar: Homonymous hemianopia Bilateral visual impairment Hemiparesis, hemisensory symptoms, diplopia, vertigo, vomiting, dysarthria, dysphagia, ataxia
210
What are the signs of TIA?
Neuro exam may be normal bc TIA may have resolved Check pulse for irregular rhythm - AF Carotid bruits
211
How is TIA investigated?
Bloods: FBC, U+E, lipids, LFTs, TSH Urinanalysis - glycosuria ECG - AF or previous MI Unenhanced CT - if possibility of haemorrhage Investigate for source of emboli - ECG/doppler US of carotid and vertebral arteries
212
How is TIA managed?
Acute neuro symps resolved completely within 24h - 300mg aspirin immediately Assessed urgently within 24h Confirmed TIA: Clopidogrel - 300mg loading dose + 75mg thereafter High-intensity statin therapy - atorvastatin 20-80mg ``` Secondary prevention: Antiplatelets AntiHTNs Lipid-modifying Tx AF Mx ```
213
How do you assess future stroke risk in TIA patients?
ABCD2 score
214
What are the possible complications of TIA?
Recurrence | Stroke
215
Summarise the prognosis for TIA patients?
Very high risk of stroke in first month after TIA and up to a year afterwards

Y3 (20 decks)

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