Neuro Flashcards
MS definition
Age of onset. Gender
Classification
Chronic autoimmune inflammatory demyelinating disorder of the CNS. Dissemination in time and space
Onset ~30yo. More females
Classification
- Relapsing-remitting (85%): Relapses, followed by remissions and periods of stability. In early stages, symptoms may go completely during remissions. After several relapses, residual damage to CNS results in only partial recovery during remissions
- Secondary progressive: Onset of MS is RR pattern but later neurological function gradually worsens, continued relapses. ~ 25% of RR progress to SP within 6y, and 50% within 15y of disease onset
- Primary progressive (10/15%): Steady progression and worsening from onset minus remissions
MS clinical presentation
Tingling
Eye (optic neuritis)
Ataxia + other cerebellar signs
Motor (usually spastic paraparesis)
Optic neuritis
- Initial presentation in 25%
- Partial/total unilateral visual loss over a few days. Often preceded by or with pain, particularly on movement
- Signs: reduced visual acuity of central vision. May be RAPD
Transverse myelitis
- Motor - weakness below level of inflammation, clumsiness, tonic spasms
- Sensory symptoms – Numbness, tingling , burning , Lhermitte’s phenomena (shock sensation radiation down the spine induced by neck flexion), altered temperature sensation
- Sphincter: Urinary urgency, frequency, hesitancy, retention, incontinence, constipation, faecal incontinence, erectile dysfunction
Cerebellar symptoms
- Symptoms and signs such as ataxia, vertigo, clumsiness, and dysmetria
Brainstem syndromes
- Ataxia
- Eye movement abnormalities that cause: diplopia, oscillopsia, nystagmus
- Bulbar muscle problems –> dysarthria or dysphagia
MS diagnosis
Management
Clinical: 2 or more attacks affecting different parts of the CNS: dissemination in time and space and exclusion of other possible causes.
DO bloods to exclude other diagnosis
- MRI: Multiple white matter plaques often perpendicular to lateral ventricles
- LP: IgG oligoclonal bands in CSF
- Visual evoked potential: Delayed auditory, visual and sensory
Management
- Symptomatic
- Fatigue: Modafinil
- Depression: SSRI
- Pain: Pregablin, Gabapentin
- Spasticity: Baclofen
- ED: Sildenafil
- Urgency/frew: Oxybutynin, tolterodine - Acute relapses
- Methylpred 1g/day IV or high dose oral for 3 days - Preventing relapses
- DMARDs: IFNb (in RR MS) or Glatiramer
- Biologics: Alemtuzumab (anti CD25), Natalizumab (anti VLA-4), Ocrelizumab (anti CD20 only one effective in PP MS)
Transverse myelitis definition
Causes
Management
Acute inflammatory disorder affecting the spinal cord with cord swelling and loss of function, characterised by development of motor weakness, sensory impairment, and autonomic dysfunction
Causes
•MS and neuromyelitis optica spectrum disorders: most common cause
•Para-infectious: Viral (e.g. HSV, CMV, EBV, HIV, rabies), Bacterial or fungal (e.g. Mycoplasma pneumonia, TB, syphilis, Lyme disease)
•Systemic autoimmune: SLE, Sjogren’s
•Systemic inflammatory: Sarcoidosis
•Paraneoplastic syndromes
Management Acute neurological deficits: •Methylprednisolone e.g. 1g/day IV for 3-5 days •If no response: Plasmapheresis •Supportive care and acute rehabilitation for all o DVT prophylaxis o Analgesia o Observe respiratory parameters
Define myasthenia gravis
Associations
Pathophysiology
Clinical presentation
Triggers
Chronic autoimmune disorder of the post-synaptic membrane at the NMJ in skeletal muscle
More common in young women
Associations
- Thymic disease
- RhA
- SLE
Pathophysiology
Circulating antibodies against the nicotinic AChR and associated proteins impair neuromuscular transmission –> weakness & fatiguability of the skeletal muscles
Clinical presentation
- Ptosis (bilateral)
- Diplopia
- Proximal limb weakness - increasing muscular fatigue with repetitive use throughout the day
- Weakness worsened by pregnancy, infection, emotion, exercise
- Sensory exam normal
Crisis = SOB severe enough to need mechanical ventilation
Triggers Beta blocker Penicillamine Procainamide Lithium Phenytoin Antibiotics e.g. gentamicin, macrolides, quinolones, tetracyclines
Myasthenia gravis investigations
Management
•Bloods
o Anti-AChR antibodies: +ve in 80%
o MuSK (muscle specific kinase) antibodies
•Serial pulmonary function tests aka SPIROMETRY: low FVC and NIF in MG crisis
•Tensilon test: give edrophonium (short-acting anti-cholinesterase) and see if it improves power
•EMG: Decrement in amplitude of compound muscle action potential following repetitive stimulation
•Thymus imaging: Image chest with CT or MRI for thymic hyperplasia/tumour (removal may improve the condition in some cases
Management •Oral Anticholinesterase: Pyridostigmine (cholinergic SE: salivation, lacrimation, sweats etc) •Immunosuppression: Prednisolone for relapses, azathioprine, methotrexate. Plasmapheresis or IVIg oStepped up (rather than normal weaning with steroids) as may be temporary exacerbation of symptoms before therapeutic effect •Thymectomy: If thymoma or no thymoma (If 18-65yo and pyridostigmine not working)
Myasthenic crisis: Intubation + mechanical ventilation + plasma exchange/IV Ig +/- Corticosteroid
Lamberton- Eaton myasthenia syndrome definition
Pathophysiology
Clinical presentation
Investigations
Management
Autoimmune disorder of the NMJ, often associated with small cell carcinoma of the lung
Pathophysiology
- Antibodies directed against VGCC: less influx of Ca2+ during presynaptic excitation –> less Ach release from presynaptic nerve terminals
Clinical presentation
Weakness but opposite of MG
o Leg weakness early (before eyes) i.e. gait difficulty
o Extra: Autonomic (dry mouth, constipation, impotence) and areflexia
o Movement improves symptoms of hyporeflexia and weakness
o Small response to edrophonium
Investigations
•EMG: Incremental increase of the compound muscle action potential after repetitive stimulation
• Anti-VGCC Abs +ve
• Chest CT scan: look for malignancy esp of lung
AChR antibodies and edrophonium testing negative
Management
•3,4 diaminopyridine (blocks K channels in nerve terminals –> increase in Ach release) or IVIg
• Regular CXRs, high resolution CTs as symptoms may precede Ca by 4yrs
Radial nerve palsy
Where does radial nerve originate from?
Where is it usually injured
What does it supply?
Symptoms
Signs
Investigations
Management
Origantes frim C5-T1
Supplies:
Triceps, Brachioradialis, Supinator, Wrist, Finger extensors, Long thumb abductor
Usually injured at shaft of humerus
Saturday night palsy
Symptoms
- Awake with wrist drop and finger drop
- Usually not aware of any sensory symptoms
Signs
- Wrist + finger drop
- Beware of false weakness of finger abduction because of finger position when wrist dropped
- May have subjectively altered light touch and pin over dorsum of hand at base of thumb and index and middle fingers
Investigations
- Nerve conduction studies
- Routine blood tests
- Consider hereditary tendency to pressure palsies (v rare)
Management
- Alcohol counselling, don’t drink until recovered
- Reassure that temporary - will recover fully in 4 weeks. Come back if only partially recovered in 4 weeks
- Splint to keep hand up
- Exercises e.g. play with ball
Nerve conduction studies + MRI if return in 4 weeks with no improvement
Median nerve palsy
Symptoms
Signs
Causes
Management
Carpal tunnel syndrome
Symptoms
- Aching pain in hand and arm worse at night
- Paraesthesia in thumb, index and middle fingers often relieved by shaking and massaging the hand
- Can be accompanied by pain in forearm
Signs
- May be none
- Wasting of thenar eminence, Weakness of APB
- May have altered sensation (light touch and pin) over index and middle finger and median half of ring finger
- Tinel’s sign
- Phalen’s sign
Causes
- Iidopathic = most common
- Water: Pregnancy, hypothyroid
- Radial fracture
- Inflammatory: RA
- Soft tissue swelling: Lipomas, acromegaly, amyloidosis
- Toxic: DM, EtOH
Management
Conservative - ergonomics e.g. wrist rests. taking breaks
Non-op - splints and corticosteroid injection. Move on to op if no improvement within 6 weeks
Op - Carpal tunnel decompression by division of flexor retinaculum. (Only one hand at a time and complications - scar and compression again)
Ulnar nerve palsy
Symptoms
Signs
Investigations
Management
Symptoms
- Numbness or tingling over ulnar border of hand and ring and little fingers
- Pt may notice tendency to drop objects
Signs
- Altered subjective sensation to light and pin over little finger and ulnar half of ring and ulnar border of hand
- Wasting of FDI (pudge sign)
- Wasting of ADB (hypothenar eminence)
- Froment’s sign (excess thumb flexion when pinching)
Investigations
- Nerve conduction studies
Management
- Surgical decompression or anterior transpostion can be performed
C spine assessment in trauma
Canadian C-spine rule: Clinically clears cervical spine fracture without imaging
- Any high risk factor which mandates radiography? Do it
- Age 65 or more
- Dangerous mechanism
- Paraesthesia in extremities - Any low risk factor which allows safe assessment of range of motion? If not, radiograph
- Simple rear end motor collision
- Sitting in ED
- Ambulatory at any time
- Delayed onset of neck pain
- Absence of midline c-spine tenderness
- -> if yes - Able to actively rotate neck? If able, no radiography
- 45 degrees left and right
Spinal cord tracts - which colour matter?
What are the 3 tracts,
Which direction do they go
What info to they carry
Where to they cross
White matter peripheral tracts
1) Lateral corticospinal
Enables intricate, strong organised movement
- originates in motor cortex neurones and terminates on motor nuclei of CN and anterior horn cells
- Crosses in medulla and pass to contralateral spinal cords, which then synapse with anterior horn cells
THIS IS KNOWN AS PYRAMIDAL SYSTEM - disease of which = UMN lesion
2) Dorsal
Light touch, Proprioception, Vibration, 2 point discrimination
- Ascend uncrossed to medulla. axons from 2nd order neurones cross midline and pass to thalamus
3) Spinothalamic
Pain and temperature
- Fibres synapse in dorsal horn of the cord, cross midline and ascend as the spinothalamic tracts to the thalamus
Spinal cord compression causes
Most common?
Presentation
Investigation
Most common = vertebral body neoplasms
- Mets from lung, breast, prostate, kidney or myeloma
- Myeloma
- Lymphoma
Disc and vertebral lesions - trauma, chronic degenerative
Inflammatory - epidural abscess, TB (Pott’s paraplegia)
Spinal cord neoplasms - primary (glioma, NF), Mets
Rarities - Paget’s disease, Bone cysts, epidural haemorrhage
Presentation
- Progressive weakness and UMN pattern and eventual paralysis in legs
- Arms affected if lesion above T spine
- Sensory level 1/2 spinal cord segments below level of compression
- May be loss of sphincter control and urinary incontinence
- May be painless urinary retention and constripation later
Investigation
- MRI
Management of spinal cord compression
Differentials
MRI - identify site and cause
Initial
- Surgical decompression of cord + stabilise spine
- Dexamethasone reduces oedema around lesion
- Think about VTE prevention
- Maintain volume and BP
- Support as needed - nutrition, ventilation, catheter
Further management depends on cause
Differentials
- Intrinsic lesion of the cord
- Transverse myelitis, anterior spinal artery occlusion and MS may present with rapid onset of paraparesis
- More insidious onset of weakness: MND (no sensory deficit), subacute combined degeneration of cord + non metastatic malignancy
Syringomyelia and syringobulbia - define
Where is lesion
Presentation
Management
Fluid filled cavity (syrinx) within spinal cord and brainstem respectively
Most lesions between C2 and T9
Presentation
- Spinothalamic (pain and temperature) loss i.e. loss of crossing fibres but preservation of dorsal columns - in a cape like distribution in upper limbs
- Unilateral/bilateral Horner syndrome
- Wasting + weakness in small muscles of hand due to damage of anterior horn cells at T1 level (common site for syrinx)
- Spastic paraparesis develops only after cavity markedly distended and compresses on corticospinal tracts
Management
MRI
Surgical decompression of foramen magnum sometimes slows down deterioration
What is freidrich’s ataxia
AR hereditary condition in fraxtin gene on Chr 9
Fraxtin found in spinal cord, heart and pancreas
Presentation
- Progressive degeneration of the posterior columns, corticospinal tract and dorsal and ventral spinocerebellar tract (proprioception)
- Ataxia - spreading from distal legs
- Dysarthria
- Nystagmus
- Dysdiadochokinesis
- Sensory neuropathy: Absent ankle jerk, absent joint position and vibration sense
- Pyramidal signs: Upgoing plantar (despite absent ankle jerk), weakness
Other features
– Optic atrophy
– Pes cavus and scoliosis
– Cardiomyopathy + associated arrhythmias
– Diabetes
Management
- No cure
- Treat CCF, arrhythmia and DM
Absent ankle jerk + Extensor planter response causes
1) Combined pathology e.g. cervical spondylosis + peripheral neuropathy
2) MND
3) Subacute combined degeneration of the cord (Fit B12 myelopathy)
4) Freidreich ataxia
5) Tabes dorsalis/tertiary neurosyphillis
Types of MND
Worst and best prognosis
Diagnosis
Management
1) Progressive muscular atrophy - mainly LMN (best prog)
2) Amytrophic lateral sclerosis - classic UMN + LMN
3) Progressive bulbar and pseudo bulbar palsy (worst prog)
4) Primary lateral sclerosis - solely UMN
NO SENSORY SIGNS OR MOTOR INVOLVEMENT OF EYE OR SPHINCTERS
Diagnosis = clinical
- Supported by EMG: Denervation
- Nerve conduction studies: Reduction in motor nerve conduction amplitude
Management - no cure, need counselling
Drugs: RILUZOLE = gultamate receptor antagonist - only 2/3 months extra survival
Supportive care
- ST + communication aids
- PT, splints, walking aids + wheelchairs
- Spasticity: Baclofen or gabapentin
- Dysphagia: Blend food
- Excess saliva: Position, oral care, suctioning. Try anti-muscarinic
- Involve palliative care
Prognosis
<3yrs post onset in most
What is amyotrophic lateral sclerosis
MND type
Combo of disease of lateral corticospinal tracts and anterior horn cells
Presentation
- Spastic tetra paresis or paraparesis with added LMN (wasting + fasciculation’s) i.e. UMN + LMN
(LMN = muscle cramps, fasiculations inc tongue, wasting and weakness)
- Onset tends to be focal, distal, asymmetrical and progress from one limb to another
NB often a mixed bulbar and pseudo bulbar picture
What is progressive bulbar and pseudo bulbar palsy
Type of MND - destruction of upper (pseudo bulbar) and Lowe (bulbar) motor neurone in the lower CNs (IX-XII)
Pseudobulbar = UMN lesion of muscles of swallowing and talking
- Dysarthria, dysphagia
- Tongue small and spastic, no dasiculations
- Exaggerated jaw jerk
- Emotionally labile
Causes: Cerebrovascular disease, MND, MS
Bulbar = LMN of tongue and muscles of swallow/talk - Dysphagia, dysarthria - Flaccid fasciculation tongue - Jaw jerk absent/normal - Speech quiet, hoarse or nasal Causes: MND, GBS, Syringobulbia, MG
Sciatic nerve - roots
Supply to what
What does it divide into
Sacral plexus (L4-S3) Supplies hip extensors and knee flexors
2 parts to the sciatic nerve
1) Common peroneal (posterior) further divides:
- Superficial: Ankle eversion
- Deep: Toe and dorsiflexion
2) Tibial nerve (anterior)
- ankle inversion and plantar flexion
RAdiculopathy definition
Causes
Presentation
Spinal nerve root lesion
Causes
- Cervical and lumbar spondylosis (degenerative changes inc. disc prolapse and osteophytes)
- Trauma
- Tumours (NF, neuroma, lymphoma, mets)
- HZV (Shingles)
- Meningeal infiltration + inflammation
- Arachnoiditis
Presentation
1) Pain: Severe, sharp, shooting, burins into dermatome or myotome supplied by root.
- Aggravated by movement, strain or cough
- May arise from soft tissue and joints also
2) Neuro signs
- LMN signs: Wasting, fasciculations, flaccid weakness and reduced/absent reflexes in affected myotome
- Sensory impairment in affected dermatome
C7 nerve
Myotome
Reflex
Dermatome
Myotome: Wrist flexion, elbow extension
Reflex = Triceps
Dermatome = Middle finger
NB need to add other nerve roots
causes of cauda equina
Differentials
Disc prolapse - most common at L5/S1 and L4/L5
Trauma e.g. vertebral fractures and subluxation
Neoplasm - primary or mets from lung, breast, kidney, prostate, thyroid
Infection e.g. discitis of Potts disease
Chronic spinal inflammation e.g. AS
Iatrogenic e.g. haematoma secondary to spinal anaesthesia
Differentials
- Radiculopathy: radiating back pain but no faecal, urinary or sexual dysfunction
- cord compression - surgical emergency but UMN signs
cauda equina symptoms and signs
tests to do
Management
Severe bilateral back pain Reduced LL sensation Bladder/bowel dysfunction (esp urinary retention) LL motor weakness Impotence
o/e
- Perianal anaesthesia aka saddle
- Loss of anal tone (PR)
- LL weakness and loss of reflexes
- Urinary retention’s
Tests
- PR
- Post void bladder scan
- whole spine MRI
Management
- Early neurosurgical review for urgent decompression
- High dose steroids e.g. dexamethasone to reduce any localized swelling
- In cases caused by malignancy, radio/chemotherapeutic can be used
Migraine requirements to diagnose
A At least 5 attacks fulfilling criteria B-D
B Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)
C Headache has at least two of the following characteristics:
1. unilateral location*
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
D During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia
E Not attributed to another disorder (history and examination do not suggest a secondary headache disorder or, if they do, it is ruled out by appropriate investigations or headache attacks do not occur for the first time in close temporal relation to the other disorder)
NICE criteria the following points are noted:
NICE suggests migraines may be unilateral or bilateral
NICE also give more detail about typical auras:
Auras may occur with or without headache and:
are fully reversible
develop over at least 5 minutes
last 5-60 minutes
Status epilepticus management
Immediate: ABC, High flow Oxygen, BM, temperature
5 mins - No IV access - Buccal midazolam 0.5mg/kg - Iv access - IV lorazepam 0.1mg/kg Gain IV access if not already. Send blood samples
15 mins - IV lorzepam 0.1mg/kg This step should be in hospital Call for senior help Start to prepare phenytoin for 4th step Re-confirm it is an epileptic seizure
25 mins
- Phenytoin 20 mg/kg by intravenous infusion over 20 mins
or (if on regular phenytoin)
- Phenobarbital 20 mg/kg intravenously over 5 mins
45 mins
Rapid sequence induction of anaesthesia using thiopental sodium 4 mg/kg intravenously
Trigeminal neuralgia
Symptoms
Red flags
Management
Trigeminal neuralgia is a pain syndrome characterised by severe unilateral pain.
Causes
The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur
Red flags
- Sensory changes
- Deafness or other ear problems
- History of skin or oral lesions that could spread perineurally
- Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
- Optic neuritis
- A family history of multiple sclerosis
- Age of onset before 40 years
Management
- Carbamazepine is first-line
- failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
What is restless leg syndrome
Causes
Diagnosis
Management
Syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia.
Symptoms/signs
Uncontrollable urge to move legs (akathisia).
Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
Paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)
Causes/associations
- FH
- iron deficiency anaemia
- uraemia
- diabetes mellitus
- pregnancy
Diagnosis = clinical but do FBC to exlude Fe deficiency anaemia
Management
- Simple measures: walking, stretching, massaging affected limbs
- Treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
- Benzodiazepines
- Gabapentin
Alternative to clopidogrel post TIA
Dual antiplatelet with aspirin + modified release dipyramidole
Proplem with clopidogrel is usually GI e.g. diarrhoea
Features of a Posterior inferior cerebellar artery stroke
AkA
Ipsilateral: facial pain and temperature loss, Horner syndrome, Ataxia, nystagmus
Contralateral: limb/torso pain and temperature loss
Lateral medullary syndrome
Wallenberg syndrome
Most commonly survived stroke that affects the brainstem
Mechanisms of damage to peripheral nerves
What do the nerve conduction studies show for main 2
1) Demyelination (Schwann Cell damage –> slowing of conduction) caused by pressure e.g. entrapment or by inflammation e.g. GBS
Nerve conduction: Decreased conduction velocity
2) Axonal degeneration: Conduction velocity initially normal. Typical in toxic neuropathies
Nerve conduction: Decreased amplitude of impulse
- Compression: Focal demyelination at point of compression –> disruption of conduction e.g. Carpal Tunnel Syndrome
- Infarction: Micro-infarction of vasa nevorum occurs in diabetes and arteritis. Wallerian degeneration occurs distal to infarct
- Infiltration: By inflammatory cells in leprosy, granulomas (e.g. sarcoid) and by neoplastic cells
Investigations for a peripheral nerve disorder
Blood: FBC, ESR, CRP, U&Es (renal function), LFTs, Glucose, Autoantibodies, Vit B12, Serum protein electrophoresis
Nerve conduction studies;
Axonal degeneration = reduced amplitude
Demyelination = reduced conduction velocity
Also characterise whether sensory and/or motor fibres involved and localise site of abnormality
EMG
Fine need inserted into muscle to discern whether partial or complete innervation present and if re–innervation occuring
Nerve biopsy
Sural nerve most commonly as purely sensory and so resulting deficit is trivial
Can confirm vasculitis or other inflammatory process
CSF
May be helpful in GBS or CIDP, when protein raised, without inflammatory cells
Mononeuritis multiplex define
Causes
Investigations
2 or more peripheral nerves affacted
Causes : WAARDS PLC W = Wegener's A = Aids A = Amyloid R = RA D = DM = most common S = Sarcoidosis P = PAN L= Leprosy C = Carcinomatosis
Investigations - as for peripheral nerve disorders + EMG helps define site of lesion:
Blood: FBC, ESR, CRP, U&Es (renal function), LFTs, Glucose, Autoantibodies, Vit B12, Serum protein electrophoresis
Nerve conduction studies;
Axonal degeneration = reduced amplitude
Demyelination = reduced conduction velocity
Also characterise whether sensory and/or motor fibres involved and localise site of abnormality
EMG
Fine need inserted into muscle to discern whether partial or complete innervation present and if re–innervation occuring
Nerve biopsy
Sural nerve most commonly as purely sensory and so resulting deficit is trivial
Can confirm vasculitis or other inflammatory process
CSF
May be helpful in GBS or CIDP, when protein raised, without inflammatory cells
Ulnar nerve motor and sensory innervation
Ulnar nerve palsy causes
Motor
1) Flexor carpi ulnaris
2) Flexor digitorum profundus
Then all small muscles of hand except APB. OPB, Lateral 2 lumbricals and part of FPB
Sensory
Ulnar 1 and 1/2 fingers
Causes of ulnar nerve palsy
Entrapment usually at elbow here nerve compressed within cubital tunnel, which lies behind medial epicondyle
- Can follow ulnar fracture
- Micro injury by leaning on elbow
- Vibrating tools and cyclists
- Stretching of ulnar nerve e.g. sleeping with elbow bent to more than 90degrees
Common peroneal nerve injury causes
Presentation
Differentials
Management
Causes
- Most common is fibular neck injury due to compression e.g. surgical positioning, crossing legs, trauma
Presentation - Weakened dorsiflexion, foot drop - Weakened foot eversion So foot inverted and foot drop Numb dorsum of foot + lateral lower leg
Differentials
- L5 radiculopathy: Weakened dorsiflexion, weakened foot eversion, weak foot inversion, weakened hip internal rotation _ abduction. Numbness over dorsum and lateral leg
- Sciatic nerve injury: Weakness of dorsiflexion. plantar flexion, foot eversion, foot inversion
- Cortical lesion: UMN signs e.g. babinski reflex present
Management
Conservative: PT, orthopaedic devices e.g. splints
Medical: Corticosteroid injections may help, neuropathic pain treatment
Surgical: If disorder doesn’t go away
L5 nerve root
Dermatomes
Myotome
Reflex
Myotome: Long toe extensor
Dermatome: On the dorsum of the foot at the third metatarsal phalangeal joint.
Reflex
Causes of bilateral foot drop
1) Peripheral neuropathy
2) Bilateral radiculopathy but more commonly..
3) Cauda equine syndrome/ Conus medullaris syndrome
4) MND
5) Spastic paraplegia
GBS define
Cause
Pathophysiology
Classification
Guillan barre syndrome = Acute inflammatory demyelination polyradiculoneuropathy (AIDP)
Cause
No precipitant in 40%; 1-3 weeks after rest infections/diarrhoea (campylobacter esp)
Pathophysiology
Infecting organisms induce antibody responses against peripheral nerves
Classification
- AIDP
- AMAN (acute motor (+/- sensory) axonal neuropathy)
- Miller fisher: Opthalmoplegia (ocular muscle palsies) + ataxia + areflexia
GBS presentation
Investigations
Management
Prognosis
Weakness and sensory loss progress proximally, ASCENDING over days/weeks
- Often starts with sensory loss
Loss of tendon reflexes = almost invariable
In mild cases, spontaneous recovery begins but in 20% resp failure and fascial muscles become weak, sometimes progressing to complete paralysis
Autonomic features may develop: Arrhythmias, Tachy, Labile BP, Sweating, Urinary retention; Constipation
Investigations
- Nerve conduction studies: Demyelinating (AFTER 10d)
- Image spine to ensure no Cauda equina
- LP shows high protein!! + normal cells (AFTER 1 week)
- FVC - worry if downward trajectory (ITU if below 1)
- Assess swallow
- Continuous heart monitoring
Management
- IVIg 1st line (check IgA first as deficiency can –> bad reaction)
- Plasma exchange
NO STEROIDS
Prognosis
Recovery graduate but occurs in 80%
What is CIDP
Management
Chronic inflammatory demyelinating polyradiculopathy
- Clinical features and pathology similar to GBS but rarely preceding infection
- Often milder syndrome than GBS
Management
- Corticosteroids +/- immunosuppression
What is Charcot Marie tooth syndrome
Presentation
Investigations
Management
Hereditary motor and sensory neuropathy. Usually AD
CMT1 = demyelinating with hypertrophy of nerves CMT2 = Axonal degeneration
Presentation
- onset at puberty
- Distal wasting over lower limbs –> champagne bottles
- Pes cavus
- 1/3 have postural tremor
- 1/2 have thickening of peripheral nerves
- Absent ankle jerk
- Sensory features not as marked as motor
Investigations
- Genetic tests: PMP22 gene mutation
- Nerve conduction studies - reduced velocity in CMT1
Management = Supportive
PT/OT/Podiatry/ Orthoses (ankle braces)
Botulism toxin
Prevents ACh vesicle release
Presentation
- Descending flaccif paralysis
- Anti-cholinergic effects: Mydriasis, Cycloplegia, Day mouth, Constipation
Management
Benpen + antiserum
Stroke pathophysiology
Ischaemic due to infarct (85%)
1) Vascular: Thrombotic; Large artery stenosis; Small vessel disease (lacunar)
2) Cardioembolic (30% of stroke)
- AF/arrhythmia; Endocarditis/valve disease; MI; PFO
3) Haem
Hyoperfusion (severe hypotension e.g. Cardiac arrest may lead to infarction in watershed areas between vascular territories); Prothrombotic hyper coagulable states
Intracerebral haemorrhagic stroke
HIgh BP; Trauma; Aneurysm rupture; Anticoagulants; Thrombolysis
Other
- Watershed stroke (sudden drop in BP e.g. sepsis)
- Carotid artery dissection
- Vasculitis - PAN/HIV
- Cerebral vasospasm secondary to SAH
- Venous sinus thrombosis
- Anti-phospholipid syndrome, thrombophillia
Stroke clinical classification system
- Total anterior circulation stroke (TACS)
- Total anterior circulation stroke (TACS)
Large cortical stroke affecting the areas of the brain supplied by both the MCA and ACA
All three of the following need to be present for a diagnosis of TACS:
• Unilateral weakness (and/or sensory deficit) of the face, arm and leg
• Homonymous hemianopia
• Higher cerebral dysfunction (dysphasia, visuospatial disorder) - Partial anterior circulation stroke (PACS)
Less severe form of TACS, in which only part of the anterior circulation has been compromised.
Two of the following need to be present for a diagnosis of PACS:
• Unilateral weakness (and/or sensory deficit) of the face, arm and leg
• Homonymous hemianopia
• Higher cerebral dysfunction (dysphasia, visuospatial disorder) - Posterior circulation syndrome (POCS)
Damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).
One of the following need to be present for a diagnosis of POCS:
• Cranial nerve palsy and a contralateral motor/sensory deficit
• Bilateral motor/sensory deficit
• Conjugate eye movement disorder (e.g. horizontal gaze palsy)
• Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
• Isolated homonymous hemianopia - Lacunar syndrome (LACS)
Subcortical stroke that occurs 2 to small vessel disease. No loss of higher cerebral functions (e.g. dysphasia).
One of the following needs to be present for a diagnosis of LACS:
• Pure sensory stroke
• Pure motor stroke
• Senori-motor stroke
• Ataxic hemiparesis
The homonymous hemianopia is always the same side as the hemiplegia!!
What are the Parkinson’s plus syndromes
5 Vivid red flags to unfurl
1) Early postural instability and vertical gaze palsy ± falls; rigidity of trunk > in limbs; symmetrical onset; speech and swallowing problems; little tremor→ progressive supranuclear palsy: (PSP, Steele–Richardson–Olszewski syndrome).
2) Neurology Early autonomic features, eg impotence/incontinence, postural ↓ bp; cerebellar + pyramidal signs; rigidity > tremor→multiple system atrophy (msa; Shy–Drager).
3) Neurology Fluctuating cognition with visual hallucinations and early dementia→Lewy body dementia ([link]).
4) Neurology Akinetic rigidity involving one limb; cortical sensory loss (eg astereognosis); apraxia (even autonomous interfering activity by affected limb—the ‘alien limb’ phenomenon)→cortico-basal degeneration (cbd).
5) Neurology Pyramidal signs (legs), eg in diabetic/hypertensive patient who falls247 or has gait problems, eg ataxia (no festination)→vascular parkinsonism (2–5% of ‘pd’).
Bitemporal hemianopia
Where is lesion
Cause and how do they present differently
Homonymous hemianopia
- Where is lesion and what are causes
Bitemporal hemianopia = lesion at optic chiasm
- Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
- Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
Homonymous hemianopia
- Incongruous defects: lesion of optic tract
- Congruous defects: lesion of optic radiation or occipital cortex
- Macula sparing: lesion of occipital cortex
Main points
1) Left homonymous hemianopia means visual field defect to the left, i.e. Lesion of right optic tract
2) Homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
3) Incongruous defects = optic tract lesion; congruous defects = optic radiation lesion or occipital cortex
Cluster headaches management
Triggers
Acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes)
Prophylaxis: Verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone
NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging
Trigger: alcohol
CNS tumours
What are the majority?
Diagnosis
Management
- 60% = Glioma and metastatic disease
20% = Meningioma
10% = Pituitary lesions
In paediatric practice medulloblastomas (neuroectodermal tumours) were the commonest lesions, astrocytomas now account for the majority.
Tumours arising in right temporal and frontal lobe may reach considerable size before becoming symptomatic. Whereas tumours in the speech and visual areas will typically produce early symptoms.
Diagnosis
MRI Scanning provides the best resolution.
Treatment
Dexamethasone can be used to reduce oedemax
Usually surgery, even if tumour cannot be completely resected conditions such as rising ICP can be addressed with tumour debulking and survival and quality of life prolonged.
- Curative surgery can usually be undertaken with lesions such as meningiomas.
- Gliomas have a marked propensity to invade normal brain and resection of these lesions is nearly always incomplete.
Epilepsy
Localising features of focal seizures
Temporal lobe (HEAD)
- Hallucinations (auditory/gustatory/olfactory),
- Epigastric rising/Emotional,
- Automatisms (lip smacking/grabbing/plucking),
- Deja vu/Dysphasia post-ictal)
Frontal lobe (motor) - Head/leg movements, posturing, post-ictal weakness, Jacksonian march
Parietal lobe (sensory) Paraesthesia
Occipital lobe (visual) Floaters/flashes
Normal pressure hydrocephalus
Presentation
Causes
Imaging
wet, wobbly and whacky
= urinary incontinence, gait ataxia, and dementia respectively.
Causes
Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients.
- It is thought to be secondary to reduced CSF absorption at the arachnoid villi.
- These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.
Imaging
Hydrocephalus with an enlarged fourth ventricle
Typically an absence of substantial sulcal atrophy
Management
- Ventriculoperitoneal shunting
- Around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages
Internuclear opthalmoplegia
Cause
Presentation
Occurs due to a lesion of the medial longitudinal fasciculus (MLF), a tract that allows conjugate eye movement.
- Vascular disease
- MS
Features
- Impaired adduction of the eye on the same side as the lesion
- Horizontal nystagmus of the abducting eye on the contralateral side
Tuberous sclerosis
Presentation
Tuberous sclerosis (TS) is a genetic condition of autosomal dominant inheritance. Like neurofibromatosis, the majority of features seen in TS are neurocutaneous.
Cutaneous features
Depigmented ‘ash-leaf’ spots which fluoresce under UV light
Roughened patches over lumbar spine (Shagreen patches)
Adenoma sebaceum (angiofibromas): butterfly distribution over nose
Fibromata beneath nails (subungual fibromata)
café-au-lait spots* may be seen
Neurological features
developmental delay
epilepsy (infantile spasms or partial)
intellectual impairment
Also
retinal hamartomas: dense white areas on retina (phakomata)
rhabdomyomas of the heart
gliomatous changes can occur in the brain lesions
polycystic kidneys, renal angiomyolipomata
lymphangioleiomyomatosis: multiple lung cysts
Neurofibromatosis T1
vs
T2
Type 1 - CAFE SPOT
Cafe-au-lait spots Axillary, inguinal freckling Fibroma Eye: Lisch nodules (iris) Skeletal: bowing leg Pedigree/FH : AD Optic tumour(glioma)
T1 has peripheral predominance
T2 has central predominance
Type 2
- Few skin/skeletal malformation
- Vestibular schwannomas/ CNS tumours
Migraine triggers
Migraine management
The mnemonic CHOCOLATE is useful for remembering the common precipitants.
Chocolate Hangovers Orgasms Cheese Caffeine The oral contraceptive pill Lie-ins Alcohol Travel Exercise
Management
acute: triptan + NSAID or triptan + paracetamol
Prophylaxis: topiramate or propranolol
- Topiramate is also recommended by NICE as first-line prophylaxis against migraine. However, in female and of child-bearing age a beta-blocker (such as propranolol) is a better choice.
Meningioma
Where do they arise from?
Location
Histology
Investigation
Management
The second most common primary brain tumour in adults
- Meningiomas are typically benign, extrinsic tumours of the central nervous system. They arise from the dura mater of the meninges and cause symptoms by compression rather than invasion.
- They typically are located at the falx cerebri, superior sagittal sinus, convexity or skull base.
- Histology: Spindle cells in concentric whorls and calcified psammoma bodies
- Investigation is with CT (will show contrast enhancement) and MRI, and
- Treatment will involve either observation, radiotherapy or surgical resection.
Vestibular schwannomma
Location
Presentation
Which NF are they associated with?
Investigation
Management
Vstibular schwannomas (sometimes referred to as acoustic neuromas) account for approximately 5% of intracranial tumours and 90% of cerebellopontine angle tumours.
The classical history of vestibular schwannoma includes a combination of vertigo, hearing loss, tinnitus and an absent corneal reflex.
Features can be predicted by the affected cranial nerves:
cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy
Bilateral vestibular schwannomas are seen in neurofibromatosis type 2.
Patients with a suspected vestibular schwannoma should be referred urgently to ENT. It should be noted though that the tumours are often slow growing, benign and often observed initially.
MRI of the cerebellopontine angle is the investigation of choice. Audiometry is also important as only 5% of patients will have a normal audiogram.
Management is with either surgery, radiotherapy or observation.
Wernicke’s encephalopathy
Presentation
Treatment
Risk
Cause
Alcohol - B1 (thiamine deficiency)
Triad:
1) Ophthalmoplegia/nystagmus,
2) Ataxia and
3) confusion may occur
Treatment = Pabrinex
If not treated Korsakoff’s syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of
4) antero- and retrograde amnesia and
5) confabulation .
Idiopathic intracranial hypertension
Classic pt demographic
Features
Management
Classically seen in young, overweight females.
Risk factors obesity female sex pregnancy drugs*: oral contraceptive pill, steroids, tetracycline, vitamin A, lithium - tetracycline antibiotics - isotretinoin - contraceptives - steroids - levothyroxine - lithium - cimetidine
Features headache blurred vision papilloedema (usually present) enlarged blind spot sixth nerve palsy may be present
Management
weight loss
Diuretics e.g. acetazolamide
Topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
Epilepsy management
1st and 2nd line drugs for the following:
Generalised tonic clonic
Absence seizures
Myoclonic seizures
Focal seizures
Most neurologists now start antiepileptics following a second epileptic seizure. NICE guidelines suggest starting antiepileptics after the first seizure if any of the following are present:
the patient has a neurological deficit
brain imaging shows a structural abnormality
the EEG shows unequivocal epileptic activity
the patient or their family or carers consider the risk of having a further seizure unacceptable
Sodium valproate is considered the first line treatment for patients with generalised seizures with carbamazepine used for focal seizures.
Generalised tonic-clonic seizures
sodium valproate
second line: lamotrigine, carbamazepine
Absence seizures* (Petit mal)
sodium valproate or ethosuximide
sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy
Myoclonic seizures**
sodium valproate
second line: clonazepam, lamotrigine
Focal seizures
carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproate
*carbamazepine may exacerbate absence seizures
**carbamazepine may exacerbate myoclonic seizures
Subdural haemorrgage
Appearance on CT
CT: Crescents
Source of bleeding: Shearing of bridging veins between cortex and venous sinus.
3rd nerve palsy
Features
Causes
Features
eye is deviated ‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)
Causes diabetes mellitus vasculitis e.g. temporal arteritis, SLE false localizing sign* due to uncal herniation through tentorium if raised ICP --- eep posterior communicating artery aneurysm pupil dilated often associated pain cavernous sinus thrombosis
Weber’s syndrome:
= ipsilateral 3rd palsy with contralateral hemiplegia -caused by midbrain strokes
other possible causes: amyloid, multiple sclerosis
GCS
Motor response
- Obeys commands
- Localises to pain
- Withdraws from pain
- Abnormal flexion to pain (decorticate posture)
- Extending to pain
- None
Verbal response
- Orientated
- Confused
- Words
- Sounds
- None
Eye opening
- Spontaneous
- To speech
- To pain
- None
C8
Myotome
Reflex
Dermatome
Myotome: Finger flexors
Dermatome: On the dorsal surface of the proximal phalanx of the little finge
Brain abscess
Causes
Symptoms
Imaging
Treatment
Causes: Many
1) Extension of sepsis from middle ear or sinuses
2) Trauma or surgery to the scalp
3) Penetrating head injuries and embolic events from endocarditis
The presenting symptoms will depend upon the site of the abscess (those in critical areas e.g.motor cortex) will present earlier.
Raised ICP signs
Although fever, headache and focal neurology are highly suggestive of a brain abscess the absence of one or more of these does not exclude the diagnosis, fever may be absent and even if present, is usually not the swinging pyrexia seen with abscesses at other sites.
Assessment of the patient includes imaging with CT scanning . MRI: Diffusion restricting!
Treatment is usually surgical, a craniotomy is performed and the abscess cavity debrided. The abscess may reform because the head is closed following abscess drainage.
Rules about stopping epilepsy treatment
Can stop if seizure free for >2 years and withdraw over 2-3 months
What is an ataxic gait
Causes
Wide-based gait, loss of the heel to toe pattern and instability.
Causes - cerebellar injury (PASTRIES) Posterior fossa tumour Alcohol S Multiple sclerosis Trauma Rare causes Inherited (Freidrich's ataxia) Epilepsy treatments Stroke
Essential tremor
Symptoms
Management
Essential tremor (previously called benign essential tremor) is an autosomal dominant condition which usually affects both upper limbs
Features
postural tremor: worse if arms outstretched
Improved by alcohol and rest
Most common cause of titubation (head tremor)
Management
propranolol is first-line
primidone is sometimes used
MRC grading of power
Grade 0 No muscle movement
Grade 1 Trace of contraction
Grade 2 Movement at the joint with gravity eliminated
Grade 3 Movement against gravity, but not against added resistance
Grade 4 Movement against an external resistance with reduced strength
Grade 5 Normal strength
Levodopa
Use
Adverse effects
Overview
usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine
reduced effectiveness with time (usually by 2 years)
no use in neuroleptic induced parkinsonism
Adverse effects Dyskinesia 'On-off' effect Postural hypotension Cardiac arrhythmias nausea & vomiting Psychosis reddish discolouration of urine upon standing
Phenytoin
use
MOA
Adverse effects
Phenytoin is used in the management of seizures.
Mechanism of action
binds to sodium channels increasing their refractory period
Adverse effects
Phenytoin is associated with a large number of adverse effects. These may be divided into acute, chronic, idiosyncratic and teratogenic. Phenytoin is also an inducer of the P450 system.
Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures
Chronic
common: !!!gingival hyperplasia!!! (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
!!Peripheral neuropathy!!
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia
Idiosyncratic fever rashes, including severe reactions such as toxic epidermal necrolysis hepatitis Dupuytren's contracture* aplastic anaemia ???Drug-induced lupus???
Teratogenic
associated with CLEFT PALATE and congenital heart disease
Monitoring
Phenytoin levels do not need to be monitored routinely but trough levels, immediately before dose should be checked if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication
Types of aphasia following stroke
Where is lesion
What is speech like
What is comprehension like
Broca’s (expressive) aphasia
- lesion of the inferior frontal gyrus.
- It is typically supplied by the superior division of the left MCA
- Speech is non-fluent, laboured, and halting
- Comprehension is normal
Wernicke’s (receptive) aphasia
- lesion of the superior temporal gyrus.
- It is typically supplied by the inferior division of the left MCA
This area ‘forms’ the speech before ‘sending it’ to Broca’s area. Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent
- Comprehension is impaired
Conduction aphasia
- Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area
- Speech is fluent but repetition is poor. Aware of the errors they are making
- Comprehension is normal
Global aphasia
Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia
Dopamine receptor agonists
Examples
Side effects
e.g. bromocriptine, ropinirole, cabergoline, apomorphine
Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with
- pulmonary, retroperitoneal and cardiac fibrosis.
- -> echocardiogram, ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored
Potential for IMPULSE CONTROL DISORDERS and excessive daytime somnolence
More likely than levodopa to cause hallucinations in older patients.
Nasal congestion and postural hypotension are also seen in some patients
Complications of meningitis
Neurological sequalae Sensorineural hearing loss (most common) Other neurological: epilepsy, paralysis Infective: sepsis, intracerebral abscess Pressure: brain herniation, hydrocephalus
Which anti-emetics for which conditions
Haloperidol for intracranial causes (raised ICP, direct effect of tumour)
Prochlorperazine for vestibular causes
Metoclopramide for gastrointestinal causes
Sodium valproate side effects
P450 Inhibitor Gastrointestinal: nausea Increased appetite and WEIGHT GAIN Alopecia: regrowth may be curly Ataxia Tremor Hepatotoxicity Pancreatitis Thrombocytopaenia Teratogenic hyponatraemia hyperammonemic encephalopathy: L-carnitine may be used as treatment if this develops
Opiod misuse
Features
Opiod examples
Features rhinorrhoea needle track marks pinpoint pupils drowsiness watering eyes yawning
Complications
Viral infection secondary to sharing needles: HIV, hepatitis B & C
Bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis
Venous thromboembolism
Overdose may lead to respiratory depression and death
psychological problems: craving
Social problems: crime, prostitution, homelessness
Opioids are substances which bind to opioid receptors. This includes both naturally occurring opiates such as morphine and synthetic opioids such as buprenorphine and methadone
Cocaine adverse effects
MOA
Cardiovascular effects myocardial infarction both tachycardia and bradycardia may occur hypertension QRS widening and QT prolongation aortic dissection
Neurological effects seizures mydriasis hypertonia hyperreflexia
Psychiatric effects
agitation
psychosis
hallucinations
Others ischaemic colitis is recognised in patients following cocaine ingestion. This should be considered if patients complain of abdominal pain or rectal bleeding hyperthermia metabolic acidosis rhabdomyolysis
Mechanism of action
cocaine blocks the uptake of dopamine, noradrenaline and serotonin
LP contraindications
Thrombocytopenia Lateness Pressure Unstable Coagulation disorder Infection at LP site Neurology (focal near signs)
GCS <9 or a drop of 3 or more
Key signs in meningitis
Kernig’s: Straightening leg ̄c hip @ 90
Brudzinski’s: lifting head → lifting of legs
Suspected meningitis Investigations
Meningitis CSF findings
Management
Investigations suggested by NICE full blood count CRP coagulation screen blood culture whole-blood PCR blood glucose blood gas
Lumbar puncture if no signs of raised intracranial pressure
Bacterial: Cloudy; Glucose low (<1/2 plasma), Protein high (>1g/l), WCC 10-5,000 polymorphs
Viral: Clear/cloudy, Glucose (60-80% of plasma), Protein normal/raised, WCC 15-1,000 lymphocytes
TB: Slight cloudy, Glucose low (1/2 plasma), Protein high (>1g/l), WCC 10-10,000 lymphocytes
Abx therapy
Community: benpen 1.2g IV/IM
<50: ceftriaxone 2g IVI/IM BD
>50: ceftriaxone + ampicillin 2g IVI /4h If viral suspected: aciclovir
Dexamethasone 0.15mg/kg IV QDS - reduced neuro sequelae
Encephalitis
Features
Causes
Investigations
Management
Features
fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to presence of HSV encephalitis
Pathophysiology
HSV-1 responsible for 95% of cases in adults
typically affects temporal and inferior frontal lobes
Investigation
CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz
Management
Intravenous aciclovir should be started in all cases of suspected encephalitis STAT - 10 mg/kg every 8 hours for at least 14 days in encephalitis
Phenytoin for seizures
Raised ICP signs
Causes
Headache n/v Seizures Drowsiness → coma Cushing’s reflex: ↑BP, ↓HR, irregular breathing 6th CN palsy (may be false localising) Cheyne-Stokes respiration Pupils – constriction → dilatation Papilloedema, loss of venous pulsation @ disc
Causes Haemorrhage Tumours Infection: meningitis, encephalitis, abscess Hydrocephalus Status Cerebral oedema
Head injury indications to CT
CT head immediately GCS < 13 on initial assessment GCS < 15 at 2 hours post-injury suspected open or depressed skull fracture. any sign of basal skull fracture (haemotympanum, 'panda' eyes, cerebrospinal fluid leakage from the ear or nose, Battle's sign). post-traumatic seizure. focal neurological deficit. MORE than 1 episode of vomiting
CT head scan within 8 hours of the head injury - for adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury:
age 65 years or older
any history of bleeding or clotting disorders
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury
If a patient is on warfarin who have sustained a head injury with no other indications for a CT head scan, perform a CT head scan within 8 hours of the injury
Erbs palsy
Presentation
Nerves affected
Pronated and medially rotated
brachial trunks C5-6.
Triptan use
Prescribing point
Adverse effects
CIs
riptans are specific 5-HT1B and 5-HT1D agonists used in the acute treatment of migraine. They are generally used first-line in combination therapy with an NSAID or paracetamol.
Prescribing points
should be taken as soon as possible after the onset of headache, rather than at onset of aura
oral, orodispersible, nasal spray and subcutaneous injections are available
Adverse effects
‘triptan sensations’ - tingling, heat, tightness (e.g. throat and chest), heaviness, pressure
Contraindications
patients with a history of, or significant risk factors for, ischaemic heart disease or cerebrovascular disease
Anterior vs middle cerebral artery stroke picture
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
Middle cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Brain herniation cause
Types
As intracranial pressure rises to pathological levels, normal brain structures are forcefully displaced. This is called herniation.
Subfalcine
Displacement of the cingulate gyrus under the falx cerebri
Central
Downwards displacement of the brain
Transtentorial / uncal herniation
Displacement of the uncus of the temporal lobe under the tentorium cerebelli.
Clinical consequences include an ipsilateral fixed, dilated pupil (due to parasympathetic compression of the third cranial nerve) and contralateral paralysis (due to compression of the cerebral peduncle)
Tonsillar
Displacement of the cerebellar tonsils through the foramen magnum.
This is called ‘coning’.
In raised ICP this causes compression of the cardiorespiratory centre.
In Chiari 1 malformation, tonsillar herniation is seen without raised ICP
Transcalvarial
Occurs when brain is displaced through a defect in the skull (e.g. a fracture or craniotomy site)
