Neurology Flashcards
(223 cards)
1
Q
Brain metastases epidemiology
A
- 55% malignant
- 3% of all cancers - 9th most common
- Common differential diagnosis
- In adults - majority supratentorial
- In children - majority in posterior fossa
2
Q
Brain metastases types
A
- Over 150 types
- Primary:
- Meningioma - tumour of brain lining
- Paediatric - germ cells, sellar region
- Gliomas - tumours of intrinsic brain
- Carnal nerve tumours e.g. acoustic neuroma
- Lymph cell tumours - primary CNS
- Secondary:
- Matastatic tumours from lung, breast, colorectal, testicular, renal cell, malignant melanoma
3
Q
Brain metastases classification
A
- WHO classification - histology
- 1 - neuroepithelial tumours (most common)
- Astrocytic - most common
- Oligodendroglial - IDH-1 mutation positive
- Ependymal - line the ventricles and spinal cord
- Neuronal and neuro-glial
- Pinela
- Embryonal
- Choroid Plexus
- 2
- Cranial and spinal nerve tumours
- Meningeal tumours - second most common
- Lymphomas - without evidence of systemic disease
- Germ cell tumours - within brain
- Metastatic tumours
4
Q
Brain metastases WHO grading
A
- WHO grading I-IV
- I - Pilocytic astrocytoma, good prognosis, completely benign, mainly in children
- II - Diffuse astrocytoma, >5yr prognosis, premalignant tumour
- III - Anaplastic astrocytoma, 2-5yr prognosis, malignant, will see active growth and mitotic activity on microscope
- IV - Glioblastoma Multiforme (GBM), <1yr prognosis, will show active growth, mitotic activity, necrosis and vascular proliferation
5
Q
Brain metastases causes
A
- Majority no cause
- Ionising radiation
- 5% family history
- Immunosuppression
6
Q
Brain metastases symptoms
A
- Cancer symptoms - weigth loss, malaise, loss of appetite
- Raised ICP headache - worse in morning or lying down
- Seizures - happens in 80%, type depends on where tumour is
- Focal neurological symptoms - progressive over days to weeks, depends on region of tumour
- Papilloedema - swelling of optic disc from venous obstruction from raised ICP
7
Q
Brain metastases differential diagnosis
A
- Aneurysm
- Abscess
- Cyst
- Haemorrhage
- Idiopathic Intracranial Hypertension
8
Q
Brain metastases investigations
A
- MRI - will show high grade tumours, irregular mass with vasogenic oedema
- Biopsy - using frame-based/frameless stereotactic
- Low grade gliomas - look at cerebral blood volume, MR spectroscopy (composition), rate of growth, bloods, molecular markers (IDH mutation, ATRX loss, TP53 mutation)
9
Q
Brain metastases treatment
A
- High grade - dexamethasone (reduce oedema), biopsy or resection, radiotherpat, chemotherapy (temozolamide, PCV)
- Low grrade - resection or biopsy, radiotherapy alone (delays progression), radio and chemo (improves survival)
10
Q
Cauda Equina epidemiology
A
- Rare
- Occurs in 2% of herniated discs
- Can occur at any age
11
Q
Cauda Equina pathology
A
- Nerve root compression caudal (distal) to the termination of the spinal cord at L1/L2
- Usually large central disc herniation at L4/L5 or L5/S1 levels (sciatica)
- Generally, S1-S5 nerve root compression – important in bladder function
12
Q
Cauda Equina causes
A
- Herniation of lumbar disc - mostly L4/L5 and L5/S1
- Spondylolisthesis - slippage of one vertebra over the one below so effects root below
- Trauma
- Tumour
- Infection
- Post-op haematoma
13
Q
Cauda Equina Symptoms
A
- Saddle anaesthesia (perineum, perianal, medial legs and thigh)
- Less bladder and bowel control - increased tone of anal sphincter and bladder muscle wall, urinary retention
- Erectil dysfunction
- Lumbosacral pain
- Lew weakness - flaccid and areflexic (absence of deep tendon reflexes)
- Paraplegia
14
Q
Cauda Equina differential diagnosis
A
- Conus medullaris syndrome
- Vertebral fracture
- Peripheral neuropathy
- Mechanical back pain
15
Q
Cauda equina investigations
A
- MRI spine
- Exam:
- Knee flexion - tests L5-S1
- Ankle plantar flexion - S1-S2
- Straight leg raising - L5-S1
- Femoral stretch test - L4
16
Q
Cauda Equina management
A
- Refer to neurosurgeon asap
- Surgical decompression
- High dose dexamethasone
- Corticosteroids
17
Q
Cauda Equina red flags
A
- Bilateral sciatica - pain, weakness, numbness, tingling
- Bilateral flaccid leg weakness
- Saddle anaesthesia
- Bladder and bowel dysfunction
- Erectile dysfunction
- Areflexia
18
Q
Acoustic neuroma description
A
- Benign tumours of the schwann cells surrounding the auditory nerve that innervates the inner ear.
- Occur at the cerebellopontine angle
- Usually unilateral.
- Bilateral ones are associated with neurofibromatosis type II
19
Q
Acoustic neuroma presentation
A
- Typically aged 40-60
- Unilateral sensorineural hearing loss
- Unilateral tinnitus
- Dizziness or imbalance
- A sensation of fullness in the ear
20
Q
Acoustic neuroma investigations
A
- Audiometry assess hearing loss
- Brain imaging is used to establish the diagnosis (MRI gives more detail than CT)
21
Q
Acoustic neuroma management
A
- Conservative - monitor
- Surgery - remove tumour
- Radiotherapy - to reduce growth
Risks:
- Vistibulocochlear nerve injury with permanent hearing loss or dizziness
- Facial nerve injury with facial weakness
22
Q
Bells palsy presentation
A
- Unilateral lower motor neurone facial nerve palsy
- Forehead will be paralysed.
23
Q
Bells palsy management
A
- Majority fully recover in week, can take a year. A third are left with residual weakness
- If present within 72 hours, give prednisolone
- Lubricating eye drops prevents drying out and damage
- Pain in the eye needs opthalmology review for exposure keratopathy
24
Q
Cerebral palsy description
A
- Permanent neurological problems resulting from damage to the brain around the time of birth.
- Not progressive but symptoms may change over time
- Wide variety in severity and symptoms
25
Cerebral palsy causes
- Antenatal - maternal infection, trauma during pregnancy
- Perinatal - birth asphyxia, pre-term birth
- Postnatal - meningitis, severe neonatal jaundice, head injury
26
Cerebral palsy types
- Spastic: hypertonia and reduced function resulting from damage to upper motor neurones
- Dyskinetic: problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems resulting from damage to basal ganglia
- Ataxic: problems with coordinated movement resulting from damage to the cerebellum
- Mixed: a mix of spastic, dyskinetic and/or ataxic features
27
Cerebral palsy patterns
- Monoplegia: one limb affected
- Hemiplegia: one side of the body affected
- Diplegia: four limbs are affects, but mostly the legs
- Quadriplegia: four limbs are affected more severely, often with seizures, speech disturbance and other impairments
28
Cerebral palsy presentation
- Children at risk (with hypoxic-ischaemic encephalopathy) need to be followed up for symptoms developing.
Signs and symptoms:
- Failure to meet milestones
- Increased or decreased tone, generally or in specific limbs
- Hand preference below 18 months is a key sign to remember for exams
- Problems with coordination, speech or walking
- Feeding or swallowing problems
- Learning difficulties
29
Cerebral palsy examination
Gait
- Hemiplegic/ diplegic gait: indicates an upper motor neurone lesion
- Broad based gait/ ataxic gait: indicates a cerebellar lesion
- High stepping gait: indicates foot drop or a lower motor neurone lesion
- Waddling gait: indicates pelvic muscle weakness due to myopathy
- Antalgic gait (limp): indicates localised pain
- Upper motor neurone - muscle bulk preserved, hypertonia, slightly reduced power, brisk reflexes
- Lower motor neurone - reduced muscle bulk with fasciculations, hypotonia, dramatically reduced power, reduced reflexes
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Cerebral palsy complications
- Learning disability
- Epilepsy
- Kyphoscoliosis
- Muscle contractures
- Hearing and visual impairment
- Gastro-oesophageal reflux
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Cerebral palsy management
- Management will involve a multi-disciplinary team approach
- Physiotherapy - stretch and strengthen muscles, maximise function
- Occupational therapy - help manage everyday activities and help make adaptations and supply equipment
- Speach and language therapy - help with speech and swallowing, help with NG or PEG tubes
- Dieticians - ensure they meet nutritional requirements, may need tubes
- Orthopaedic surgeons - procedures to release contractures or lengthen tendons
- Paediatricians - see regularly to optimise medications (muscle relaxants, anti-epileptics, glycopyrronium bromide for excessive drooling)
- Social workers - help with benefits
- Charities and support groups
32
Encephalitis pathology
- Inflammation of brain (mainly frontal and temporal lobes), resulting in decreased consciousness, confusion and focal signs
- Mostly children and elderly
33
Encephalitis causes
- Usually viral - Herpes simplex (most common), varicella zoster (chicken pox), measles, mumps, rubella, EBV, HIB, CMV, coxsackie
- Other - TB, malaria, rabies, Japanese encephalitis, tick-borne encephalitis
- Non-infective - autoimmune, paraneoplastic
34
Encephalitis symptoms
- Flu-like symptoms - in first hours to days then:
- Altered GCS
- Fever
- Headache
- Seizures
- Memory loss
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Encephalitis differential diagnosis
- Meningitis
- Stroke
- Brain tumour
36
Encephalitis investigations
- MRI head - show swelling/inflammation and midline shifting
- EEG - periodic sharp and slow waves
- Lumbar puncture - raised lymphocytic CSF, viral PRC
- HIV test
37
Encephalitis treatment
- IV Aciclovir - if HSV or VZN
- Carbamazepine - fro seizures
- IM benzylpenicillin - if meningitis suspected
38
Describe an epileptic seizure
- Paroxysmal event of behaviour, sensation or cognitive processes change due to excessive hypersynchronous neuronal discharges in brain (too much voltage)
- 30-120secs, hallucinations, lateral tongue bite, déjà vu, eyes open, muscle pain, postictal confusion
39
Describe a non-epileptic seizure
- Paroxysmal event of behaviour, sensation and cognitive function changes by mental processes associated with psychosocial distress
- 1-20 mins, situational, eyes closed, crying or speaking
40
Describe prodrome
Prodrome - before seizure, can last hours or days, change in mood or behaviours
41
Describe aura
Aura - patient aware of it, déjà vu or hallucinations, implies partial seizure
42
Describe post-ictal
Post-ictally - headache, confusion, myalgia, sore tongue, temporary weakness after focal seizure in motor cortex (Todd’s palsy), dysphagia following focal seizure in temporal lobe
43
Describe generalised epilepsy seizures and types
- Generalised (40%) - electrical discharge through whole cortex, bilateral motor manifestations, always loss of consciousness or awareness
- Tonic - sudden stiffening
- Clonic - rhythmic muscle jerking
- Atonic - sudden loss of muscle tone and cessation
- Tonic-clonic - no aura, rigidity then jerking, post-ictal
- Absence seizure - more in childhood, patient unaware
- Myoclonic - sudden isolated jerk
44
Describe partial/focal seizures and types
- Partial/focal (57%) - features referred to a lobe
- Temporal - memory, emotion,, receptive speech, aura, automatisms (non-purposeful behaviour)
- Frontal - motor and thought processing, Jacksonian march (seizure “marches” up or down the motor homunculus starting in face or thumb), post-ictal Todd’s palsy for several hours
- Parietal - sensory, tingling/numbness
- Occipital - visual phenomena (spots, lines, flashes)
- Simple partial - remains conscious, small area of brain, often remembers
- Complex partial - loss of consciousness or impaired awareness and memory
45
Epilepsy causes
- Tumour
- Stroke
- Raised ICP
- Meningitis
- Trauma
- Hippocampal sclerosis (main cause of temporal)
- Cortical scarring (haemorrhage, infection, history of head injury)
- Flashing lights may provoke attack
46
Describe structural/metabolic epilepsy
- Associated with focal brain abnormality
- Jacksonian seizures, psychomotor, secondary generalised
- Hippocampal sclerosis
- Investigation: EEG
- Treatment: Carbamazepine or Lamotrigine
47
Describe genetic generalised epilepsy
- Usually <30
- Absence, myoclonic, primary generalised tonic seizures
- Treatment: Valproate or Lamotrigine
48
Epilepsy differentials
- Parasomnia
- TIA
- Dystonia
- Migraine
- Postural syncope
- Hyperventilation
- Hypoglycaemia
49
Epilepsy investigations
- 2 or more seizures more than 24 hours apart
- EEG
- CT head
- MRI
- Bloods - FBC, U&E, renal and liver function, glucose (rule out metabolic causes)
50
Describe epilepsy emergencies
Satus Epilepticus - seizure lasting >5 mins, usually tonic clonic, can be life-threatening
51
Epilepsy treatment
- Status epilepticus – IV lorazepam
- Generalised – sodium valproate or lamotrigine
- Partial/focal - carbamazepine
- Absence - Ethosuximide
- Resective surgery - know epileptic region and remove it (cure)
- Hemispherectomy - remove epileptic focus (cure)
- Tractotomy - stop seizure spread by cutting pathways (palliative)
- Electrostimulation - mostly vagus nerve (palliative)
- Must inform DVLA - can’t drive until seizure free for one year
52
Essential tremor description
- Common in older age
- Fine tremor affecting all voluntary muscles
- Most notable in hands also head, jaw nad vocal
53
Essential tremor features
- Fine tremor
- Symmetrical
- More prominent with voluntary movement
- Worse when tired, stressed or after caffeine
- Improved by alcohol
- Absent during sleep
54
Essential tremor differential
- Parkinson’s disease
- Multiple sclerosis
- Huntington’s chorea
- Hyperthyroidism
- Fever
- Dopamine antagonists
55
Essential tremor management
- Propranolol - non-selective beta blocker
- Primidone - barbiturate anti-epileptic medication
56
Extradural haemorrhage causes
- Traumatic head injury - mostly to temple, ruptures middle meningeal artery
- Usually young adults
57
Extradural haemorrhage pathology
- Head injury → fracture in temporal/parietal bone → laceration of middle meningeal artery
- Blood accumulates between bone and dura over mins-hours
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Extradural haemorrhage symptoms
- Headache, N&V, seizure
- Bradycardia and raised BP
- Ipsilateral pupil dilation
- Decreased Glasgow coma scale
- Coning of brain through foramen ovale
- Respiratory arrest
59
Extradural haemorrhage differential diagnosis
- Subdural haematoma
- Subarachnoid haematoma
- Epilepsy
- Meningitis
- Carotid dissection
- Carbon monoxide poisoning
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Extradural haemorrhage investigations
-
- CT - shows biconvex hypodense haematoma that is adjacent to skull
- Skull XR - may show fracture lines crossing middle meningeal artery
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Extradural haemorrhage treatment
- Refer to neurosurgeon - burr hole craniotomy and irrigation/removal of haematoma vie burr twist drill, ligation of bleeding vessel
- ABCDE management
- IV mannitol - reduces ICP
62
Giant Cell Arteritis description
- Known as temporal arteritis
- Systemic vasculitis affecting the medium and large arteries
- Strong link with polymyalgia rheumatica
- More common in older white patients
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Giant cell arteritis presentation
- Unilateral headache, severe around temple and forehead
- Scalp tenderness (when brushing hair)
- Jaw claudication
- Blurred or double vision
- Loss of vision if untreated (often irreversible)
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Giant Cell Arteritis diagnosis
- Clinical presentation
- Raised inflammatory markers
- Temporal artery biopsy - multinucleated giant cells
- Duplex ultrasound - hypoechoic ‘halo’ sign and stenosis of temporal artery
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Giant Cell Arteritis Management
- Prednisolone - 40-60mg daily with no visual symptoms or jaw claudication
- Methylprednisolone - 500-1000mg daily with visual symptoms or jaw claudication
- Aspirin - decreases vision loss nad strokes
- PPI - for gastro protection while on steroids
- Bisphosphonates and calcium and vit D - for bone protection while on steroids
66
Giant Cell Arteritis Complications
- Steroid-related - weight gain, diabetes, osteoporosis
- Visual loss
- Stroke
67
Guillian-Barre syndrome Epidemiology
- More males
- Peak ages 15-35 and 50-75
- Most common acute polyneuropathy
68
Guillian-Barre syndrome pathology
- Some infectious organisms have same antigens as on Schwann cells → autoantibody mediated damage to myelin sheath via molecular mimicry → reduction in peripheral nerve conduction → acute polyneuropathy
- Types: Demyelinating, axonal, axonal sensorimotor, Miller Fisher syndrome (rare, affects cranial nerves to the eye)
- Recovery in several months due to myelin sheath regrowth
69
Guillian-Barre syndrome causes
- Bacterial - campylobacter jejuni, mycoplasma pneumoniae
- Viral - CMV, EBV, Zoster, HIV
70
Guillian-Barre syndrome risk factors
- History of resp or GI infection 1-3 weeks prior
- Post pregnancy - decreases in pregnancy but increases months after delivery
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Guillian-Barre syndrome symptoms
- Paraesthesia and numbness
- Muscle weakness - symmetrical ascending
- Back and limb pain
- CN involvement - diplopia and dysarthria
- Resp - affects diaphragm → death
- Autonomic - sweating, raised pulse, postural hypotension, arrhythmias
72
Guillian-Barre syndrome differential diagnosis
- Hypokalaemia
- Polymyositis
- Myasthenia gravis
- Botulism
- Poliomyelitis
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Guillian-Barre syndrome investigations
- Lumbar puncture at L4 - CSF has normal WBC, raised protein
- Nerve conduction studies - slow conductoin, prolonged distal motor latency and conduction block (diagnostic with clinical exam)
- Spirometry - monitor FVC, decrease = urgent ITU admission
74
Guillian-Barre syndrome treatment
- IV Immunoglobulin - decreases duration and severity of paralysis (not with IgE deficiency)
- Plasmapheresis - filter out antibodies
- LMW heparin and compression socks reduce risk of venous thrombosis
75
Herpes Zoster epidemiology
- 90% of children exposed before 16
- Incidence and severity increases with age
- Shingles can’t be caught from someone with chicken pox
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Herpes Zoster risk factors
- Old age
- Immunocompromised
- Chicken pox <18 months age
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Herpes Zoster pathology
- Viral infection affecting peripheral nerves
- Varicella (chicken pox) lies dormant in the dorsal root ganglion
- When reactivated (by herpes zoster = shingles) in travels down affected nerve via sensory root in dermatomal distribution over 3-4 days → perineural and intramural inflammation
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Herpes Zoster symptoms
- Dermatomal distribution of rash (of papules and vesicles) and pain, crust formation and drying over a week and resolves in 2-3 weeks
- Malaise, myalgia (muscle ache), headache, fever
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Herpes Zoster differential diagnosis
- Atopic eczema
- Contact Dermatitis
- Herpes simplex
- Cluster headaches
- Migraine
80
Herpes Zoster treatment
Oral Aciclovir
81
Huntington's disease chorea description
- Huntington’s is a cause of chorea and is aneurodegenerative disorder characterised by the lack of the main inhibitory neurotransmitter GABA
- Continuous flow of involuntary jerky, semi-purposeful movements
82
Huntington's disease epidemiology
- Autosomal dominant condition with full penetrance - all gene carriers will develop disease
- Presents in middle age
- Rare
83
Huntington's disease pathology
- Mutation on chromosome 4 → repeat CAG sequence leads to translation of expanded polyglutamine repeat sequence in huntingtin gene - more repeats mean earlier symptoms
- Faulty Huntingtin protein builds up in striatum causing cell death and loss of cholinergic and GABA-nergic neurons → decreased ACH and GABA synthesis
- Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
- Need >36 triplets to be diagnostic
84
Huntington's disease symptoms
- 1st phase - depression, incoordination, personality changes
- 2nd phase - chorea, abnormal eye movements, loss of coordination, dysarthria (weak speech muscles), dysphagia (difficulty swallowing), dementia, depression, rigidity
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Huntington's disease differentials
- Sydenham’s chorea (rheumatic fever)
- SLE
- Basal ganglia stroke
- Wilson’s disease
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Huntington's disease investigations
- Genetic testing - shows CAG repeats
- MRI/CT - atrophy of striatum (caudate and putamen) and increased size of frontal hrons of lateral ventricles
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Huntington's disease treatment
- No cure
- Chorea - antipsychotics (Risperidone) are dopamine receptor antagonists. Benzodiazepines. Sulpriride depresses nerve function
- Depression - SSRIs
- Aggression - antipsychotic
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Hypoxic-ischaemic encephalopathy description
- Occurs in neonates from hypoxia during birth
- Ischaemia from restriction in blood flow to the brain
- Encephalopathy refers to malfunctioning of the brain
- Prolonged can lead to permanent damage and cerebral palsy.
89
Hypoxic-ischaemic encephalopathy red flags
May suspect HIE when there are events that could cause hypoxia
- acidosis on the umbilical artery blood gas
- Poor Apgar score
- Evidence of multi organ failure
90
Hypoxic-ischaemic encephalopathy causes
- Maternal shock
- Intrapartum haemorrhage
- Prolapsed cord
- Nuchal cord (cord wrapped around baby’s neck)
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Hypoxic-ischaemic Encephalopathy staging
- Mild: Poor feeding, generally irritability and hyper-alert, resolves within 24 hours, normal prognosis
- Moderate: poor feeding, lethargic, hypotonic and seizures, can take weeks to resolve, up to 40% develop cerebral palsy
- Severe: reduced consciousness, apnoeas, flaccid and reduced or absent reflexes, up to 50% mortality, up to 90% develop cerebral palsy
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Hypoxic-ischaemic Encephalopathy management
- Supportive care in neonatology - ventilation, circulatory support, nutrition, acid base balance, treatment of seizures
- Therapeutic hypothermia - occassionally used to protect from hypoxic injury
- Followed up by multidisciplinary team to assess development
93
Hypoxic-ischaemic encephalopathy therapeutic hypothermia
- Actively cooling the core temperature of the baby with cooling blankets and a cooling hat.
- Transferred to neonatal ICU
- Target between 33 and 34 degrees using a rectal probe.
- Conitnued for 72 hours then gradually warmed over 6 hours
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Meniere's disease pathophysiology
Excessive build up of endolymph in the labyringth of the inner ear
Endolymphatic hydrops is the high pressure cause disrupting sensory signals
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Meniere's disease presentation
- 40-50 years
- Unilateral episodes of vertigo, hearing loss and tinnitus
- Vertigo - in episodes, last for 20mins-hours. Not triggered by movement or posture
- Hearing loss - fluctuates at first then becomes more permanent. Sensorineural hearing loss, generally unilateral and affects low frequencies first
- Tinnitus - initially with episodes of vertigo before becoming permanent
- Other symptoms - fullness in ear, unexplained falls, imbalance
96
Meniere's disease diagnosis
Clinical based on symptoms by an ENT
97
Meniere's disease management
- Managing symptoms during acute attack - prochlorperazine, antihistamines
- Prophylaxis - betahistine
98
Meningitis epidemiology
- More common in infants, young children and elderly
- Meningococcal disease is a notifiable disease
99
Meningitis pathology
- Bacteria get in to CSF through neurosurgical complications, extracranial infection (ear, sinuses, nasopharynx), blood stream (bacteraemic seeding)
- Bacteria multiplies in CSF as immune cells can’t cross BBB → leaky meningeal blood vessels → WBCs enter CSF → inflammation and brain swelling
100
Meningitis causes
- Bacterial:
- Strep pneumoniae - most common in adults, gram positive diplococci
- Neisseria meningitidis - gram negative diplococci, more teenagers
- Viral - Coxsackie virus, Herpes simplex, HIV, mumps, echovirus, CMV, EBV, polio (very rare)
- Parasitic - P. Falciparum
- Autoimmune - vasculitis, SLE, etc.
101
Meningitis risk factors
- Students
- Travel
- Immunosuppressed
- Pregnancy
102
Meningitis symptoms
- Fever
- Headache
- Neck stiffness
- Purpuric rash - only in bacterial. Non-blanching = meningococcal septicaemia
- Photophobia and/or phonophobia
- Papilloedema - swelling of optic disc, usually bilateral
- Kernig’s sign - lying on back with legs 90 degrees, can’t fully extend knee without causing back pain
- Brudzinski’s sign - passive flexion of neck causes flexion of both legs and thighs
- Glass test - over rash, won’t disappear
103
Meningitis differentials
- Subarachnoid haemorrhage - thunderclap onset headache
- Migraine
- Encephalitis
- Flu
- Sinusitis
- Brain abscess
- Malaria
104
Meningitis investigations
- Blood cultures before antibiotics
- Head CT - exclude lesions
- Lumbar puncture - diagnostic
- Bacterial - appears cloudy, polymorphs (neutrophils) under microscopy, organisms seen on gram film
- Viral - appears clear, lymphocytes on microscopy, no organisms seen
- TB - appears ‘fibrin web’, lymphocytes on microscopy, organisms seen on phenol auramine/Ziehl Neelson stain
105
Meningitis treatment
- Treat first
- Assess GCS - if <8 intubate
- 1st line: Cefotaxime or Ceftriaxone. Ignore penicillin allergy unless anaphylaxis then chloramphenicol
- Change to targeted antibiotic when cultures are back
- IV dexamethasone
- Prohylaxis for close contacts - Rifampicin, Ciprofloxacin
106
Meningitis complications
- Venous sinus thrombosis
- Cerebral oedema
- Cerebral abscess
107
Migraine definition
- Recurrent throbbing headache often preceded by aura and associated with N&V and visual changes
- Aura - visual: zig-zag lines, black holes. Pins and needles, dysphagia
108
Migraine epidemiology
- Most common cause of recurrent headache
- More females
- Severity usually decreases with age
- Strong genetic component
109
Migraine pathology
Changes in brainstem blood flow → unstable trigeminal nerve nuclei in basal thalamus → release of vasoactive neuropeptides (CGRP and substance P) → neurogenic inflammation, vasodilation and plasma protein extravasion
110
Migraine causes
- No known cause but triggers have mnemonic CHOCOLATE
- Chocolate
- Hangovers
- Orgasms
- Cheese
- Oral contraceptive
- Lie-ins
- Alcohol
- Tumult - loud noise
- Exercise
111
Migraine types
- Migraine without aura - 4 diagnostic criteria
- A - 5 attacks fulfilling B-D
- B - attacks last 4-72 hours
- C - two of: unilateral, pulsing, moderate/severe, aggravated by physical activity
- D - during headache at least one of: N&V, photophobia, phonophobia
- Migraine with aura - 3 diagnostic criteria
- A - at least 2 attacks fulfilling B and C
- B - >1 aura symptom: visual, unilateral sensory tingling/numbness, aphasia, motor weakness
- C - >2 of: more than one aura symptom over 5 minutes or more than 2 aura symptoms occurring in succession, aura symptom lasts 5-60mins, >1 aura symptom unilateral, aura followed within 60mins by headache
112
Migraine diferentials
- Tension headache
- Cluster headache
- Medication over-use headache
- Meningitis
- Subarachnoid haemorrhage
- Tumour
113
Migraine investigations
- Exam - eyes, BP, head and neck
- RED FLAGS - thunderclap headache, change in pattern, abnormal neurological exam, onset >50 years, epilepsy, posteriorly located headache
- Do lumbar puncture if: thunderclap, severe rapid onset, progressive, unresponsive
114
Migraine treatment
- Conservative - avoid triggers
- Acute - mild: NSAID/paracetamol + anti-emetic. Severe: oral triptan (sumatriptan)
- Prophylaxis
- 1st line - propranolol or topiramate (anti-convulsant)
- 2nd line - acupuncture
- 3rd line - amitriptyline (tricyclic anti-depressant)
- 4th line - Botulinum toxin type A (only if not responded to 3 other drugs)
115
Physiology of movement
- Upper motor neurons in 5th layers of motor cortex in pre-frontal gyrus, axons travel through spinal cord via corticospinal tract
- Lower motor neurons in motor nuclei in brain stem and go down spinal cord in columns in ventral horn of spinal grey matter
- Idea of movement → acctivation of UMNs → corticospinal tracts. Modification of movement from cerebellum and basal ganglia
- Stretch receptors in muscle (spindles) innervated by gamma motor neurons detect stretch → afferent impulses from spindles → reflex partial contraction of muscle
116
MND types
- Amyotrophic Lateral Sclerosis (ALS) - loss of MN in motor cortex and anterior horn → progressive focal wasting, weakness and fasciculaiton spreading to other limbs, UMN + LMN
- Primary Lateral Sclerosis (PLS) - UMN only. Slow progressive tetraparesis and pseudobulbar palsy
- Progressive Muscular Atrophy (PMA) - LMN only. Weakness and fasciculations starting in one limb and progressing to adjacent spinal segments
- Progressive Bulbar Palsy (PBP) - UMN + LMN + CN IX, X, XI, XII. lower cranial nerve nuclei affected causing dysarthria, dysphagia, nasal regurgitation of fluids, choking, flaccid fasciculating tongue, absent jaw jerk
117
MND epidemiology
-
- More men
- Mostly middle aged
- Most die within 3 years - usually resp failure fromo bulbar palsy and pneumonia
- Associated with SOD-1 gene
118
MND pathology
Degenerative condition affecting mainly anterior horn cells → destruction → UMN and LMN dysfunction, no sensory or sphincter loss (differs from MS), never affects eye movement (differs from MG)
119
MND symptoms
- UMN - everything goes UP
- Muscle tone increased
- Hyperreflexia
- Positive Babinski sign (stroke sole of foot, normally big toe goes down, in UMN lesion it goes up)
- Upper limb extensor weaker than flexors
- Lower limb flexor weaker than extensors
- Pyramidal drift - hold hands out one arm will drift
- LMN - everything goes DOWN
- Muscle tone normal or reduced
- Hyporeflexia
- Muscle wasting
- Respiratory muscle weakness
- Fasciculation - visible spontaneous contraction of motor units
120
MND differentials
- Cervical spine lesion - may be UMN or LMN
- Idiopathic multifocal motor neuropathy - weakness mostly in hands and profuse fasciculation
121
MND investigations
- Clinical - LMN + UMN signs in 3 regions (definite)
- UMN lesions - MRI, bloods for metabolic disorders, CSF exam (oligoclonal bands)
- LMN lesions - MRI, electromyography, bloods (raised creatinine kinase), lumbar puncture (exclude inflammatory causes)
122
MND treatment
- No cure
- Oral Rituzole - sodium channel blocker inhibits glutamate release
- Symptom management
- Dysphagia – NG/PEG tube
- Drooling (due to bulbar palsy) – oral amitriptyline or propantheline
- Spasticity – baclofen
- Joint pain – analgesic ladder
123
MS description
Chronic autoimmune, T-cell mediated inflammatory disorder (type 4 hypersensitivity) of the CNS in which there are multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years
124
MS Epidemiology
- More females
- More common further from equator
- Usually diagnosed 20-40
125
MS Pathology
- T cells cross BB and cause cascade of B cells producing auto-antibodies against myelin → discrete plaques of demyelination
- Newly regenerated myelin is less efficient and symptoms worsen in heat (Uhthoff’s phenomenon)
- Plaques are perivenular (occur around a vein) most commonly at optic nerves, ventricles of brain, corpus callosum, brainstem and cerebellar connections, cervical spinal cord.
- Active:
- Demyelination – breakdown products present
- Variable oligodendrocytes
- Hypercellular plaque edge due to infiltration of tissue with inflammatory cells
- Perivenous inflammatory infiltrate (mainly macrophages and T-lymphocytes)
- Extensive BBB disruption
- Older active plaques may have central gliosis
- Inactive:
- Demyelination – breakdown products absent
- Variable oligodendrocytes loss
- Hypocellular plaque
- Variable inflammatory infiltrate
- Moderate to minor BBB disruption
- Plaques gliosed
126
MS classification
- Pattern 1 - macrophage mediated
- Pattern 2 - antibody mediated (lots of inflammation, responds to plasma exchange)
- Pattern 3 - distal oligodendrogliopathy and apoptosis (ischaemic or virus induced)
- Pattern 4 - primary oligodendroglia degeneration (metabolic defect)
127
MS types
- Relapsing/remitting - most common. Full or partial recovery with residual deficits
- Primary progressive - progression from onset with no remission but occasional plateaus
- Secondary progressive - initial relapsing-remitting then continuous progression
- Progressive/relapsing - progressive from onset with acute relapses and time between continues progression
128
MS risk factors
- Environment
- Genetics - associated with HLA-DR2
- Exposire to EBV in childhood predisposes you
129
MS symptoms
- Depends on region affected as it affects white matter
- Charcot’s neurological triad
- Dysarthia - due to plaques in brainstem
- Intention tremor - due to plaques along motor pathways
- Nystagmus - due to plaques in nerves of eyes
- Spinal cord - Lhermitte’s sign (electric shock runs down back and radiates to limbs), bladder and sexual dysfunction, paraplegia, spasticity, numbness
- Optic nerves - impaired vision, eye pain
- Medulla and pons - dysarthria, double vision, vertigo, nystagmus
- Cerebellar white matter - dysarthria, nystagmus, intention tremor, ataxia
130
MS differentials
- SLE
- Sjogren’s
- Lyme disease
- Syphilis
- AIDS
- Cardiac embolic event
131
MS investigations
- MRI with contrast - active lesions appear white
- Lumbar puncture with CSF electrophoresis - oligoclonal IgG bands show CNS inflammation
- Evoked potentials - tests how long impulses take to travel, will be slower
132
MS treatment
- Acute attacks - IV methylprednisolone (for relapsing-remitting)
- Chronic 1st line - SC beta interferon and glatiramer acetate
- S/E flu-like symptoms, mild intermittent lymphopenia, rise in liver enzymes
- Chronic 2nd line
- IV alemtuzumab - CD52 monoclonal antibody that targets T cells
- IV natalizumab - acts against VLA-4 receptors allows immune cells cross BBB
- Tremor - beta blockers
- Muscle spasticity - diazepam (mild-moderate), phenol (peripheral nerve blocks - severe)
133
Muscular dystrophy description
Umbrella term for genetic conditions that cause gradual weakening and wasting of muscles
134
Muscular dystrophy types
-
- Duchennes muscular dystrophy
- Beckers muscular dystrophy
- Myotonic dystrophy
- Facioscapulohumeral muscular dystrophy
- Oculopharyngeal muscular dystrophy
- Limb-girdle muscular dystrophy
- Emery-Dreifuss muscular dystrophy
135
Describe gowers sign
- A specific technique children with proximal muscle weakness use to stand up from lying
- Go onto hands and knees then push hips up and backwards, put hands on knees, walk hands up legs until standing
136
Muscular dystrophy management
- No cure
- Occupational therapy, physiotherapy and medical appliances
- Surgical and medical management for spinal scoliosis and heart failure
137
Describe duchennes muscular dystrophy
- Caused by a defective gene for dystrophin on the X-chromosome, X-linked recessive
- Presentation - boys, 3-5years progressive weakness around the pelvis, wheelchair bound by teens, life expectancy of 25-35years
- Oral steroids may slow progression of muscle weakness
- Creatine supplementation can improve muscle strength
138
Describe beckers muscular dystrophy
- Dystrophin gene is less severely effected than duchennes and maintains some functions.
- Presentation 8-12years wheelchair bound in 20s or 30s
139
Describe myotonic dystrophy
- Typically presents in adulthood
- Progressive muscle weakness
- Prolonged muscle contractions
- Cataracts
- Cardiac arrhythmias
140
Describe facioscapulohumeral muscular dystrophy
- Presents in childhood with weakness around the face progressing to the shoulders and arms
- Sleep with eyes slightly open, unable to blow their cheeks out without air leaking from their mouth.
141
Describe oculopharyngeal muscular dystrophy
Presents in late adulthood with weakness of ocular muscles around the eyes and pharynx around the throat
142
Describe limb-girdle muscular dystrophy
Presents in teens with progressive weakness around limb girdles (hips and shoulders)
143
Describe emery-dreifuss muscular dystrophy
Presents in childhood with contractures (shortening of muscles restricts range of movement) in elbows and ankles. Progressive weakness and wasting of muscles.
144
Myasthenia gravis epidemiology
- More females
- Peak incidence for females 30
- Peak incidence for males 60
- Associated with other autoimmune diseases
- Associated with thymic hyperplasia in 70% and thymic tumour in 10%
145
Myasthenia gravis pathology
- Type 2 hypersensitivity reaction
- B cells produce anti-AChR autoantibodies which interfere with neuromuscular junction by binding to nicotinic AChR on muscle cells → blocks it’s excitatory effect → activation of complement pathway resulting in muscle cell destruction
- Some people produe muscle specific receptor tyrosine kinase (MuSK) antibodies which target proteins in muscle cells
146
Myasthenia gravis symptoms
- Increasing muscle weakness/fatigue improves with rest
- Ptosis (drooping eyelid)
- Diplopia (double vision)
- Bulbar - difficulty chewing and talking
- Respiratory difficulties
147
Myasthenia gravis differentials
- Thyroid opthalmology
- MS
- Myotonic dystrophy
- Brainstem cranial nerve lesions
- Lambert-Eaton myasthenic syndrome - ACh at NMJ → proximal limb weakness with absent reflexes improves after exercise
148
Myasthenia gravis investigations
- Anti-AChR antibodies in serum - found in 90% (if negative look fro anti-MuSK)
- Exam - count to 50 (voice becomes quieter), can’t keep eyes looking up
- Nerve stimulation tests - decrease in evoked potential
- Electromyography - fatiguability
- CT/MRI of mediastinum - shows thymus hyperplasia, atrophy or tumour
- Tensilon test - IV endrophonium → rapid temporary improvement in weakness
149
Myasthenia gravis treatment
- 1st line - oral pyridostigmine (acetylcholinesterase inhibitor) + prednisolone + azathioprine/methotrexate (immunosuppression) - increases ACh concentration
- Bisphosphonates - osteoporosis prophylaxis
- Thymectomy - reduces muscle weakness
- Crisses - IV immunoglobulin and plasmapheresis
150
Neurofibromatosis description
- A genetic condition that causes benign nerve tumours (neuromas)
- Can cause neurological and structural problems
151
Neurofibromatosis type 1 gene
- On chromosome 17.
- Codes for neurofibromin which is a tumour suppressor protein
- Inherited in an autosomal dominant pattern
152
Neurofibromatosis features
- C - cafe-au-lait spots
- R - Relative with NF1
- A - Axillary or inguinal freckling
- BB - Bony displasia such as Bowing of a long bone or sphenoid wing dysplasia
- I - Iris hamartomas (Lisch nodules) yellow brown spots on iris
- N - Neurofibromas
- G - Glioma of the optic pathway
153
Neurofibromatosis management
- Diagnosis based on diagnostic criteria Genetic testing can be used
- No treatment, management involves monitoring, managing symptoms and treating complications
154
Neurofibromatosis complications
- Migraines
- Epilepsy
- Renal artery stenosis
- Hypertension
- Learning disability
- Behavioural problems
- Scoliosis of the spine
- Vision loss
- Malignant peripheral nerve sheath tumours
- Gastrointestinal stromal tumour
- Brain tumours
- Spinal cord tumours
- Increased risk of cancer
155
Neurofibromatosis type 2
- Gene found on chromosome 22 it codes for merlin a tumour suppressor protein important in Schwann cells.
- Inheritance is autosomal dominant
- Lead to schwannomas, particularly associated with acoustic neuromas
- Surgery can resect tumours with risk of permanent nerve damage.
156
hydrocephalus definition
CSF building up abnormally in brain and spinal cord caused by overproduction or problem with draining or absorbing
157
Normal CSF physiology
- Four brain ventricles: two lateral ventricles, the third and the fourth
- Ventricles contain CSF to cushion brain, created in choroid plexuses
- CSF is absorbed into venous system by arachnoid granulations
158
Hydrocephalus congenital causes
- Aqueductal stenosis - most common, insufficient draignage, cerebral aqueduct connecting third and fourth ventricle is stenosed causing backup.
- Arachnoid cysts - block outflow of CSF
- Arnold-Chiari malformation - cerebellum herniates downwards through the foramen magnum blocking outflow
- Chromosomal abnormalities and congenital malformations obstruct drainage.
159
Hydrocephalus presentation
- Enlarged and rapidly increasing head circumference (occipitol-frontal circumference)
- Bulging anterior fontanelle
- Poor feeding and vomiting
- Poor tone
- Sleepiness
160
Hydrocephalus ventriculoperitoneal shunt
- VP shunts drain CSF from ventricles into another body cavity (usually peritoneal cavity)
- Catheter placed through small hole in the skull at back of head into ventricle, valve placed subcutaneously and catheter on the other side runs under the skin into peritoneal cavity
- Valve regulates the amount of CSF drained
161
Hydrocephalus - VP shunt complications
- Infection
- Blockage
- Excessive drainage
- Intrventricular haemorrhage during surgery
- Outgrowing them (need replacing every 2 years)
162
Tension headache epidemiology
- Most common primary headache
- Can be episodic (<15 days per month) or chronic (>15 days per month for at least 3 months)
163
Tension headache causes
- Neurovascular irritation which refers to scalp muscles and soft tissues
- MC SCOLD
- Missed meals
- Conflict
- Stress
- Clenched jaw
- Overexertion
- Lack of sleep
- Depression
164
Tension headache risk factors
- Stress
- Sleep Deprivation
- Bad posture
- Hunger
- Eyestrain
- Anxiety
- Noise
165
Tension headache symptoms
- A - More than 10 attacks less than 1 day per month fulfilling B-D
- B - Headache lasting 30mins-7days
- C - 2 of: bilateral, pressing/tightening quality, mild or moderate pain, not aggravated by physical activity
- D - no N&V, no more than one of photophobia or phonophobia
- E - not attributed to another disorder
166
Tension headache differentials
- Migraine
- Cluster headache
- GCA
- Drug-induced - analgesia
167
Tension headache treatment
- Stress relief - massage or acupuncture
- Paracetamol
- NSAIDS or aspirin
- Tricyclic anti-depressants - amitriptyline
168
Cluster headaches epidemiology
- Rarer than migraine
- More males
- Typically 20-40
- More common in smokers
169
Cluster headaches types
- Episodic - more than 2 periods lasting 7 days to 1 year separated by >1 month pain free periods
- Chronic - attack >1 year without remission or remission <1 month
170
Cluster headaches symptoms
- A - at least 5 attacks fulfilling B-D (diagnostic)
- B - severe or very severe unilateral orbital, supraorbital or temporal pain lasting 15-180 mins rising to crescendo
- C - accompanied by ipsilateral cranial autonomic features or sense of restlessness or agitation
- D - frequency from 1 every other day to 8 per day
- Hot poker characteristic associated with ipsilateral eye lacrimation and redness, rhinorrhoea (blocked nose), miosis (pupil constriction) or ptosis (drooping of upper eyelid)
- Usually occurs in night or morning
171
Cluster headaches treatment
- Acute - SC sumatriptan, IM zolmitriptan, 100% oxygen (unless COPD)
- Prophylaxis - Verapamil, Lithium, Corticosteroids
172
Peripheral neuropathies types
- Radiculopathy - compression of nerve root and LMN
- Mononeuropathy - affects 1 nerve (carpal tunnel, ulnar, peroneal, cranial)
- Polyneuropathy - multiple/systemic, can be motor, sensory, sensorimotor and autonomic (DM, MS, Guillain Barre)
173
Peripheral neuropathy pathology
- **Demyelination** - schwann cell damage leads to myelin sheath disruption → marked slowing of conduction (Guillain Barre)
- **Axonal Degeneration** - nerve fibre dies back from periphery. Conduction velocity initially normal because axonal continuity is maintained in surviving fibres (toxic neuropathies)
- **Compression** - focal demyelination at the point of compression causes disruption of conduction, typically in entrapment neuropathies (carpal tunnel)
- **Infarction** - micro-infarction of vasa nervorum in DM and arteritis (polyarteritis nodosa, eosiniophilic granulomatosis)
- **Infiltration** - occurs in inflammatory cells in leprosy and granulomas (cancer)
- **Wallerian degeneration** - nerve fibre is cut and distal part of axon that is separated from neuron’s body degenerates
174
Peripheral neuropathies causes
DAVID - Diabetes, Alcohol, Vit B12 deficiency, Infective, Drugs (isoniazid)
175
Peripheral neuropathies symptoms
- Sensory - A-alpha (loss of proprioception-ataxia), A-beta (loss of light touch, pressure, vibration), A-delta (loss of pain and cold), C-fibres (loss of pain and warmth)
- Motor - muscle cramps, weakness, fasciculations (twitches), muscular atrophy
- Symmetrical sensorimotor - most common, distal fibres affected first, initially sensory then sensorimotor
- Asymmetrical sensory - patchy distribution, dorsal root ganglia affected, uncommon
- Asymmetrical sensorimotor - mononeuritis multiples, very uncommon
176
Peripheral neuropathies investigations
- Exam - reduced tendon reflexes, sensory deficit, weakness
- Nerve conduction studies/QST - slow conduction velocity in demyelinating, reduced potential amplitudes in axonal
177
Peripheral neuropathies treatment
- Anti-neuralgic for pain - Gabapentin, Amitriptyline, Pregabalin
- Quinine - for cramps
- Physio for balance
178
Spinal cord compression causes
- Tumour (slow onset)
- Osteophytes
- Disc prolapse (slower onset) - nucleus pulposus moves and presses against annulus creating a bulge in the disc (less than herniation)
- Disc herniation - nucleus pulposus moves out through annulus → pressure on nerve root
179
Spinal cord compression symptoms
- UMN signs below lesion
- Sensory loss below lesion
- LMN signs at level of lesion
- Bladder sphincter involvement - hesitancy, frequency, retention
180
Spinal cord compression differentials
- Transverse myelitis
- MS
- Cord vasculitis
- Trauma
- Dissecting aneurysm
181
Spinal cord compression investigations
- Urgent MRI
- Biopsy to identify nature of mass
- CXR - if caused by TB or malignancy
182
Spinal cord compression treatment
- Surgical decompression
- Dexamethasone - reduces inflammation and oedema
183
Stroke definition
Rapid onset neurological deficits caused by focal, cerebral, spinal or retinal infarction
184
Stroke definition epidemiology
- Uncommon in <40s
- More men
- Incidence is decreasing
185
Stroke pathology
- Ischaemia stroke (85%) - atherosclerotic plaque or clot in a larger artery rupturs, travels downstream, gets trapped in a narrower artery in the brain. Embolic strokes are common complication of AF. Other causes: stenosis, vasculitis, shock
- Haemorrhagic stroke (15%) - bleeding from a single vessel in brain mainly caused by high BP, trauma or vasculitis
186
Stroke risk factors
- Black or asian
- Hypertension
- Smoking
- DM
- Past TIA
- Heart disease
- AF
187
Stroke symptoms
- MCA infarction (middle cerebral artery)
- Contralateral motor weakness, paralysis or sensory loss
- Aphasia - Wernicke’s (can’t understand) or Broca’s (can’t speak)
- Facial droop
- ACA infarction (anterior cerebral artery)
- Contralateral weakness or sensory loss in lower limb
- Incontinence
- Drowsiness
- PCA infarction (posterior cerebral artery)
- Contralateral homonymous hemianopia
- Disorders of perception
- Vertibrobasilar artery infarction
- Disorders of balance and coordination
- Posterior inferior cerebellar artery infarction
- Sudden vomiting and vertigo
- Ipsilateral Horner’s syndrome (reduced sweating, facial numbnes, dysphagia)
- Contralateral loss of pain and temperature sensation
- Haemorrhage
- Headaches
- Altered mental status
- Seizures
- N+V
188
Stroke differentials
- Hypoglycaemia
- Migrainous aura
- Mass lesions
- Syncope due to arrhythmia
- Simple partial seizures
189
Stroke investigations
- Head CT
- MRI
- CT angiography
- ECG - potential cardioembolic stroke
- Bloods - FBC (thrombocytopenia or polycythaemia), glucose (rule out hypoglycaemia), coagulation test
190
Stroke treatment
- Ischaemic - IV alteplase (within 4.5h) activates tissue plasminogen. Contraindicated in haemorrhage, clotting disorders, aneurysms
- Ischaemic - aspirin for 2 weeks then clopidogrel
- Haemorrhagic - control BP (beta blocker or ARB)
- Haemorrrhagic - surgery for clot evasion
- Rehabilitation
191
Subarachnoid haemorrhage epidemiology
- Typical age 35-65
- Account for 5% of strokes
192
Subarachnoid haemorrhage causes
- Berry aneurysm rupture (70%)
- AVM - arteriovenous malformation(10%)
- Trauma
- No cause (15%)
193
Subarachnoid haemorrhage risk factors
- Hypertension
- Known aneurysm
- Family history
- Polycystic kidney disease
- Ehler Danlos
- Coarctation of aorta
- Smoking
- Bleeding disorders
194
Subarachnoid haemorrhage pathology
- Rupture of the junction of the anterior communicating artery and the anterior cerebral artery or the posterior communicating artery and the internal carotid artery. Leads to tissue ischaemia and raised ICP → pressure on the brain → neurological deficits
- Vascular development malformation with fistula between arterial and venous systems increases blood flow → high-pressure arterialisation of draining veins → rupture
195
Subarachnoid haemorrhage symptoms
- Sudden onset severe ‘thunderclap’ headache
- Neck stiffness
- Seizures
- Vomiting
- Loss of consciousness
- Meningeal irritation - Kernig’s sign (unable to extend leg at knee when thigh is flexed)
- Brudzinski’s sign - will flex hips and knees when neck is flexed
196
Subarachnoid haemorrhage differentials
- Migraine
- Meningitis
- Corticol vein thrombosis
197
Subarachnoid haemorrhage investigations
- CT - shows bleeding withinn 24 hours
- Lumbar puncture - if CT normal but still suspect. CSF normal then yellow after a few hours due to Hb breakdown
- ABG - rule out hypoxia
198
Subarachnoid haemorrhage treatment
- Refer to neurosurgeon
- Maintain cerebral perfusion - IV fluids aim for BP >160
- Nimodipine - CCB reduces cerebral artery spasm
- Monitor for complications:
- Re-bleeding
- Cerebral ischaemia due to vasospasm
- Hydrocephalus due to blockage of arachnoid granulations
- Hyponatraemia due to urinary salt loss
199
Subdural haemorrhage epidemiology
- Common with small brains (alcoholics, dementia)
- Shaken babies
200
Subdural haemorrhage causes
- Contusions/lacerations
- Base of skull fractures
- Vertebral artery rupture
- Intraventricular haemorrhage
201
Subdural haemorrhage risk factors
- Traumatic head injury
- Age - cerebral atrophy makes bridging veins more vulnerable and more accident prone
- Alcoholics - causes cerebral atrophy
- Shaken baby syndrome
- Anti-coagulation
202
Subdural haemorrhage pathology
- Trauma from deceleration of dural metastases → bleeding from bridging veins between cortex and venous sinuses → haematoma forms (solid swelling of clotted blood) between dura and arachnoid → reduces pressure → bleeding stops
- Haematoma breaks down which increases oncotic and osmotic pressure → water sucked in → haematoma enlargement → gradual rise in ICP
- Structures in the midline shift away from clot and lead to tectorial herniation and coning (herniation through foramen magnum
203
Subdural haemorrhage symptoms
- Headache and vomiting
- Focal neurology (hemiparesis and sensory loss)
- Raised BP
- Personality change
204
Subdural haemorrhage differentials
-
- Stroke
- Dementia
- CNS masses
- Subarachnoid haemorrhage
- Extradural haemorrhage
205
Subdural haemorrhage investigations
- CT head - diffuse spreading, hyperdense crescent shaped collection of blood over one hemisphere, shifting midline structures
- MRI head
206
Subdural haemorrhage treatment
- Refer to neurosurgeon - burr hole craniotomy and irrigation/removal of haematoma via burr twist drill
- IV mannitol - to reduce ICP
207
TIA definition
Focal, sudden onset, acute loss of cerebral or ocular function <24 hours due to ischaemia without infarction
208
TIA epidemiology
- More men
- More black ethnicity
- 15% of first strokes are preceded by TIA
209
TIA pathology
- Cerebral ischaemia → lack of O2 and nutrients to the brain
- Short-live with symptoms lasting maximum 5-15 mins, resolves before irreversible cell death occurs
- 90% affect anterior circulation (carotid artery), 10% affect posterior circulation (vertebrobasilar artery)
210
TIA causes
- Atherothromboembolism from the carotid artery
- Small vessel occlusion
- Cardioembolism resulting in microemboli form
- Hyperviscosity - polycythaemia, sickle cell, high WBC, myeloma
211
TIA risk factors
- Age
- Hypertension
- Smoking
- DM
- Heart disease
- Peripheral arterial disease
212
TIA symptoms
- Sudden loss of function with complete recovery
- Stroke symptoms - slurred speech, face droop
- Carotid - Weak, numb contralateral leg or hemiparesis (weakness on one side of body), dysphasia (can’t speak), amaurosis fugax (loss of vision in one eye)
- Vertebrobasilar - diplopia (double vision), vertigo, vomiting, choking, ataxia
213
TIA differentials
- Hypoglycaemia
- Migrainous aura
- Mass lesions
- Simple partial seizures
214
TIA investigations
- ABCD2 score - risk of stroke
- A - age (>60 = 1 point)
- B - blood pressure (>140/90 = 1 point)
- C - clinical features (unilateral weakness = 2 points), (speech disturbance = 1 point)
- D - duration (>60 mins = 2 points) (10-60 mins = 1 point)
- D - Diabetes (1 point)
- High risk - score >4, AF, more than one TIA in a week, TIA whilst on anti-coagulation
- MRI
- Carotid doppler - look for stenosis
- CT angiography - look for stenosis
- ECG
215
TIA treatment
- Low risk - specialist referral within 7 days, statin (simvastatin), antiplatelet (clopidogrel), no driving
- High risk - same but assess within 24 hours
- Aspirin immediately
- Treat BP - ACEi or ARB
216
Trigeminal neuralgia epidemiology
- Peak incidece 50-60
- More females
- Almost always unilateral
217
Trigeminal neuralgia pathology
Compression of trigeminal nerve results in demyelination and excitation resulting in erratic pain signalling
218
Trigeminal neuralgia causes
- Vein or artery compressing trigeminal nerve
- Aneurysms
- Meningeal inflammation
- Tumours - vestibular schwannoma
- 5th nerve lesion
219
Trigeminal neuralgia risk factors
- Hypertension
- Triggers - washing affected area, shaving, eating, talking
220
Trigeminal neuralgia symptoms
- A - at least 3 attacks of unilateral facial pain fulfilling B and D
- B - occurring in one or more distributions of trigeminal nerve (eyes, cheek, jaw) with no radiation
- C - pain at least 3 of: reoccurring in paroxysmal attacks from 1 second to 2 minutes, severe intensity, electric shock like, precipitated by innocuous stimuli to side of face
- D - no clinically evident neurological deficit
221
Trigeminal neuralgia investigations
- Clinical diagnosis - at least 3 attacks with unilateral facial pain
- MRI - exclude secondary causes
222
Trigeminal neuralgia treatment
- 1st line - Carbamazepine (anti-convulsant)
- 2nd line - Phenytoin, Gabapentin (analgesic targeted for neuropathic pain)
- Microvascular decompression - separate blood vessels touching nerve to relieve pressure
- Stereotactic radiotherapy - deliberately damage trigeminal nerve where it enters brainstem
223
