Wk12 - Neurology Flashcards
What are the cranial nerves?
12 pairs of nerves that emerge from brainstem and supply head and neck
Sensory, motor and parasympathetic activity
I-XII
Cranial nerve abnormlaities may arise form lesions affecting..
communicating pathways to and from the cortex, cerebeluum and other part s of brainstam Nerve nucleus Nerve Neuromuscular junciton disorders Muscle
Name the 12 CNs and whether they are sensory, motor or both (parasympathetic)
And what part of the brainstem these nerves arise from
I - Olfactory - Sensory II- Optic - Sensory III - Oculomotor - Motor IV - Trochlear - Motor V - Trigeminal - Both - parasympathetic VI - Abducens - Motor VII - Facial - Both - parasympathetic VIII - Vestibulocochlear - Sensory IX - Glossopharangeal - Both - parasympathetic X - Vagus - Both - parasympathetic XI - Spinal accessory - Motor XII - Hypoglossal - Motor
Olfactory nerve
Function - smell
Tract: olfactory cells of nasal mucosa –> olfactory bulbs –> pyriform cortex
What are the nerves that move the muscles of the eye
Trochlear
Occulomotor
Abducens
Oculomotor nerve
-
Oculomotor nerve
Motor component:
Nucelus located in midbrain (oculomotor)
Function - movement of eyeball and lens accomodation
Structure innervated - inferior oblique, superior, medial and inferior recti muscles, levator palpebrae superioris
Parasympathetic component:
Nucleus located with midbrain (Edinger-Westphal)
Function: pupil constriction
Structures innervated - ciliary muscle and pupillary constrictor muscles
Trochlear nerve
Motor
Function - moves eyeball
Nucleus located in midbrain (inferior colliculus)
Structure innervated - superior oblique muscles
Depresses the adducted eye and intorts the abducted eye
Longest intracranial course
II and IV are only nerves to decussate to contralateral side
Pattern of internuclear opthalmoplegia
Disorder of conjugate gaze - failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye
Can be unilatral of bilateral
Results from lesion of medial longitudinal fasiculus
Commonly seen in multiple sclerosis
Pattern of internuclear opthalmoplegia
Disorder of conjugate gaze - failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye.
Can be unilatral of bilateral
Results from lesion of medial longitudinal fasiculus
Commonly seen in multiple sclerosis
Features seen in Horner’s syndrome
Consists of: miosis, ptosis, apparent enopthalmos, anhidrosis
Results from ipsilateral disruption of cervical/thoracic sympathetic chain:
- congenital, brainstem stroke, cluster headache, apical lung tumour, MS, carotid artery dissection, cervical rib, syringomyelia
Trigeminal nerve
Component 1 - Sensory input from face
Nucleus in pons and medulla
Structure innervated - face (ophthalmic, mandibular and maxillary division) and anterior 2/3rd of tongue
Motor component 2 - function = mastication
Nucleus located in pons
Structure innervated - masseter, temporalis, medial and lateral pterygoids
Herpes zoster ophthalmicus
Pain may precede vesicles Lifetime risk of 1% V2/V3 rarely affected Elderly and immuno-compromised at risk Treated with oral aciclovir
Facial nerve
Motor - nucleus in pons. Function - muscles of facial expression
Sensory - nucleus in medulla
Function - taste
Structures innervated - anterior 2/3 of tongue
Parasympathetic - nucleus on medulla.
Function - taste
Structure innervated - anterior 2/3 of tongue
Glossopharyngeal plasy affecting uvula…
Glossopharangeal palsy with deviation of uvula away from the side of the lesion
Spinal accessory nerve
Motor
Head rotation and shoulder
Nucles in medulla
Innervates sternocleidomastoid and trapezius muscles
Turn head against resistance - sternocleidomastoid m
Shrug shoulders
Vestibulocochlear
1 - Sensory. Function - balance. Nucleus - pons and medulla. Structure innervated - nerve endings within semi-circular canals –> cerebellum and spinal cord
2 - Sensory. Function - hearing. Nucleus in pons and medulla. Structure innervated –> auditory cortex in the temporal lobes
Mononeuropathy of ulnar nerve
Most common cause of palsy - entrapment at ulnar groovw (medial epicondyle of humerus)
Presenting symptoms - may be history of trauma; sensory disturbance and weakness (weak grip), usually painless
Motor weakness:
Glossopharangeal nerve
1 - Sensory. Nucleus in medulla. Function - taste, proprioception for swallowing, blood pressure receptors.
Structure innervated - Posterior 1/3 of tongue, pharangeal wall & carotid sinuses
2 - Motor. Nucleus in medulla. Function - swallow and gag reflex, lacrimation.
Structure innervation - pharangeal muscles, lacrimal glands
3 - Parasympathetic
Glossopharyngeal palsy affecting uvula…
Glossopharangeal palsy with deviation of uvula away from the side of the lesion
Vagus nerve
Sensory - nucleus in medulla. Function - chemoreceptors, pain receptors (dura), sensation.
Structure innervated - blood oxygen conc, carotid bodies, resp and digestive tracts, external ear, larynx and pharynx
Motor - Nucleus in the medulla. Function - heart rate and stroke volume; Peristalsis; Air flow; Speech and swallowing
Structure innervated: Pacemaker and ventricular muscles; smooth muscles of the digestive tract; smooth muscles in bronchial tubes; muscles of larynx and pharynx
Parasympathetic: Structure innervated - smooth muscles and lgands of the same areas innervated by motor component, as well as thoracic and abdominal areas
Spinal accessory nerve
Motor: Function: Head rotation and shoulder
Nucleus in medulla
Innervates sternocleidomastoid and trapezius muscles
Turn head against resistance - sternocleidomastoid muscle
Shrug shoulders - trapezius muscle
Hypoglossal nerve
Motor: Function: Speech and swallowing. Nucleus located in medulla. Structure innervated - tongue
What cranial nerves are affected by a lesion in:
Cavernous sinus Superior orbital fissure CErebellopontine angle Jugular foramen Bulbar/pseudobulbar palsy
Cavernous sinus - III, IV, V (1st and 2nd divisions), VI
Horner’s syndrome
Superior orbital fissure - III, IV, V (1st division), VI
Cerebellopontine angle - V, VII, VIII
Jugular foramen - IX, X (and XI)
Bulbar/pseudobulbar palsy - IX, X, XI (and XII)
Mononeuropathy of radial nerve
Most common cause of palsy - entrapment at spiral groove, Sat night palsy
Presenting symptoms - wrist and finger drop, usually painless
Motor weakness:
Extensor carpi radialis longus - weakness in wrist extension
Extensor digitorum communis - weakness in finger extension
Brachioradialis - weakness in elbow flexion in mid-pronation
Mononeuropathy of ulnar nerve
Most common cause of palsy - entrapment at ulnar groove (medial epicondyle of humerus)
Presenting symptoms - may be history of trauma; sensory disturbance and weakness (weak grip), usually painless
Motor weakness:
1st dorsal interosseus - weakness in index finger abduction
Abductor digiti minimi - weakness in pinkie abduction
Flexor carpi ulnaris - weakness in wrist flexion
Adductor polilicis - weakness in thumb adduction
Mononeuropathy of median nerve
Most common cause of palsy - entrapment with carpal tunnel at wrist
Presenting symptoms - history of intermittent nocturnal pain, numbness and tingling - often relieved by shaking hand; Patient may complain of ‘weak grip’; Positive Tinel’s sign/ Phalen’s test
Motor weakness:
Lumbricals I+II - weakness in flexion at MCP joints
Opponens pollicis - weakness in thumb opposition
Abductor pollicis brevis - weakness in thumb abduction
Flexor pollicis brevis -w eakness in thumb flexion
Mononeuropathy - median nerve II Anterior Interosseous branch
Most common cause of palsy - trauma to forearm
Presenting symptoms - history of forearm pain; Patient may complian of ‘weak grip’ of keys; Positive Tinel’s sign/ Phalen’s test
Motor weakness:
Pronator quadratus - weakness in flexion at MCP joints
Flexor pollicus longus - weakness in thumb flexion
Flexor digitorum profundus (lateral) - weakness in thumb flexion
Can’t do the ‘OK’ sign
What are the 3 thigh nerves
Front - femoral = quads
Medial - obturator = abduction
Back - Sciatic = Hamstrings
Mononeuropathy of femoral nerve
Most common cause of palsy - haemorrhage/trauma
Presenting symptoms - weakness of quadriceps, weakness of hip flexion and numbness in medial shin
Motor weakness:
Quadriceps - weakness in knee extension
Illiopsoas - weakness in hip flexion
Adductor magnus - weakness in hip adduction
Pathogenesis and investigation of myasthenia gravis
Autoimmune disroder: antibodies to acetylcholine receptor at post-synaptic receptor at post-synaptic NMJ
Association with other autoimmune disorders
May be associated with thymic hyperplasia or thymoma
Affects young women in 20’s and older men in 70’s
Fatigueable weakness of ocular, bulbar, neck, resp and/or limb muscles
Mononeuropathy of common peroneal nerve
Most common cause of palsy: Entrapment at fibular head (crossing legs)
Presenting symptoms: May be history of trauma, surgery or external compression; Acute onset foot drop + sensory disturbance; Usually painless
Motor weakness:
Tibialis anterior - ankle dorsiflexion
Extensor hallucis longus - Great toe extension
Mononeuritis Multiplex
Simultaneous or sequential development of 2 or more nerves.
Common causes: Diabetes, Vasculitic (Churd Strauss, polyarteritis nodosa), Rhematological (RA< lupus, Sjogren’s syndrome), Infective (Hep C, HIV), Sarcoidosis, Lymphoma
Management depends on underlying cause
Functions of PNS
Sensory input to CNS
Motor output to muscles
Innervation of viscera
Incoming sensory information enters via posterior root. Motor information exits cord via anterior root.
Collections of nerve cell bodies in PNS known as ganglia
Structure of peripheral nerves
Organisation of a peripheral nerve in fascicles and their protective connective tissue layers.
Fibre types: Large fibres (myelinated) - motor nerves; Proprioception, vibration and light touch. Thinly myelinated fibres: Light touch, pain and temperature Small fibres (unmyelinated) - light touch, pain and temperature
Anatomy of the PNS
Upper limb nerves Lower limb nerves Cervical plexus Lumbar plexus Nerve roots Neuromuscular junction and muscle
Clinical presentation of neuropathy
Motor neuropathy –> weakness/muscle atrophy
Sensory neuropathy:
Large (myelinated) fibres –> sensory ataxia, loss of vibration sense +/- numbness and tingling
Small (thinly myelinated/unmyelinated) fibres –> impaired pin prick, temperature, painful burning, numbness and tingling
Autonomic –> postural hypotension, erectile dysfunction, GI disturbance, abnormal sweating
Tendon reflexes may be reduced or absent
Length-dependednt axonal neuropathy
Limb dependent neuropathy
Starts distally and spreads proximally
‘Glove and stockings’
Age >50 years Length dependent: starts in toes/feet Symmetrical Slowly progressive No significant sensory ataxia Any weakness is distal and mild
Axon of the nerve is most commonly affected
Promdrome of migraine
Reported by 40-60%…
Acute inflammatory demyelinating neuropathy “Guillain-Barre syndrome”
Post-infectious autoimmune aetiology (e.g. campylobacter, CMV, EBV)
Progressive (ascending) weakness over days
Flaccid, quadraparesis and areflexia
+/- respiratory/bulbar/autonomic involvement
Treated with intravenous immunoglobulin or apheresis
CIDP: chronic form (steroid and IVIG responsive)
Causes demyeliantion causing weakness
Pathology is not in the axon, it is in the myelin sheath
Diagnosis of Guillian barre syndrome
Nerve conduction test ==> tests motor and sensory nerves by applying stimulation and recording the response
High protein in CSF and demyelination seen in nerve conduction test ==> diagnostic of Guillian barre syndrome
Symptoms of muscle disease
Proximal limb weakness - difficulty raising arms above head, arising from seated position
Facial weakness - myopathic facies, drolong
Eyes - ptosis, ophthalmoplegia
Bulbar - dysarthria, dysphagia
Neck and spine - head drop, scoliosis
Resp - breathlessness
Myocardial - exercise intolerance, palpitations
Causes of muscle disease
Muscular dystrophies - Dystrophinopathies (Duchenne/Becker), fascioscapulopulohumeral (FSH) dystrophy, limb girdle, oculopharyngeal
Metabolic muscle disorders - glycogen storage disease, deefcts of fatty acid metabolism
Mitochondrial disorders
Myotonic dystrophies
Inflammatory muscle disorders - Polymyositis, dermatomyositis, inclusion body myositis
Neuromuscular junction disorders - myasthenia gravis, Lambert Eaton syndrome
Pathogenesis and investigation of myasthenia gravis
Autoimmune disorder: antibodies to acetylcholine receptor at post-synaptic receptor at post-synaptic NMJ
Association with other autoimmune disorders
May be associated with thymic hyperplasia or thymoma
Affects young women in 20’s and older men in 70’s
Fatigueable weakness of ocular, bulbar, neck, resp and/or limb muscles
Investigation and management of myasthenia gravis
Antibodies to AChR present in 85% of cases
Single fibre EMG and repetitive nerve stimulation also abnormal
Managed with Pyridostigmine (anti-acetylcholine esterase) and immunosppuressive therapies (e.g. steroids and intravenous immunoglobulin).
Removal of thyroid tumour
Primary vs secondary headaches
Primary = headache and its associated features is the disorder (no underlying cause) e.g. migraine, tension-type headache, cluster headache etc.
Secondary = secondary to underlying to cause e.g. subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis, high/low intracranial pressure, drug-induced
Causes of thunderclap headache
Subarachnoid heamorrhage (approx 15% of thunderclap headache)…
Red flags suggesting secondary headache
Age>50 years
Thunderclap headache (sudden onset, strongly associated with subarachnoid haemorrhage)
Worsening of symptoms with posture change, valsalva (coughing, straining) or physical exertion (high intracranial pressure)
Early morning headahces
systemic - fever, weight loss –> worried about infection or malignancy
Seizures, meningism
Temporal artery tenderness/jaw claudication –> temporal arteritis (high levels of inflamm marker e.g. CRP, ESR)
Specific situations cause inc. risk of secondary- cancer, pregnancy, post-partum (more coagulopathic is pregnant or post-partum –> causing blood clots), HIV/immunnosuppression
SNOOPT
Systemic symptoms
Neurological signs or symptoms
Older age at onset
Onset is acute (under 5 minutes)
Previous headache history is different/absent
Triggered headache (vaslsalva or posture)
Clinical examination of patient with headache
Abnormal signs suggest secondary cause:
General/Sysgtemic:
Red. conscious level, red. pulse/BP, pyrexia, meningism, skin rash, temporal artery tenderness
Cranial nerve: Pupillary responses, visual fields +/- bind spot, eye movements, fundoscopy
Epidemiology of migraine
Female> Male
Prevalence highest aged 25-55 y/o
Positive family history
Most patients report triggers - e.g. hormonal (menstrual), weather, stress, hunger, sleep disturbance, exertion, alcohol excess, food
Types of migraine
Migraine without aura (70%)
Migraine with aurua (30%)
Migraine pathophysiology
Primary dysfunction in brainstem sensory nuclei (V, VII-X);
Pain results from pain sensitive cranial blood vessels and their innervating trigeminal fibres
Aura - cortical spreading depression
Migraine headache - activation of trigeminovascular system (with CGRP and other neuropeptides)
Phases of migraine
Prodrone - hours or days before headache ‘feel one coming on’
Aura
Headache + associated features
Postdrome
Prodrome of migraine
Reported by 40-60%
up to 48 hours before headache
Variable symptoms: mood disturbance/restlessness/hyperosmia/photophobia/diarrhoea
Aura
Recurrent reversible focal neurological symptom (e.g. visual, sensory, motor)
Develops over 5-20 mins and lasts <60 mins
Visual aura is most common (e.g. scotoma, flashing lights, fortification spectrum)
Sensory aura often starts in hand and migrates up arm
Examples of visual aura: Zigzag fortification spectrum Visual field loss Negative scotoma Positive scotoma
The headache phase of migraine
Character of headache commonly throbbing or pulsatile Moderate - severe intensity Gradual onset, duration 4-72 hours Unilateral in 60%, can radiate. Aggravated by routine physical activity
Associated symptoms of headache with migraine
Nausea and vomiting, photophobia, phonophobia, osmophobia, mood disturbance, diarrhoea, autonomic disturbance: e.g. lacrimation, conjuctival injection, nasal stuffiness
Investigation of migraine
Good history and normal clinical examination does not require further investigation
Cranial imaging advised if ‘Red Flag’ features present or aura >24 hours
Complications associated with migraine
Medication overuse headache (MOH): headache 15+ days per month associated with frequent use of acute relief medications (e.g. NSAIDs, paracetamol, opioid, analgesia, triptans) - patients advised to take acute treatments no more than 2-3 times per week to prevent MOH
Chronic headache: headache on 15+ days per month
Management of migraine
Lifestyle - avoid triggers, reduce caffeine/alcohol intake, encourage regular meals and sleep patterns
Acute management - simple analgesia (e.g. paracetamol, aspirin, NSAIDs), Triptans (e.g. Sumatriptan)
Antiemetic (e.g. metoclopramide)
Prophylaxis:
Beta-blockers (e.g. propanolol)
Tricyclic antidepressants (e.g. Amitriptyline, Nortriptiline)
Anti-epilepsy drugs (e.g. Topiramate, Sodium Valproate)
Definition of thunderclap headache
Abrupt-onset of severe headache which reaches maximal intensity >5 mins (and lasts >1hr)
‘Worst headache of life’
‘Like being hit over the head’
Should be considered as subarachnoid haemorrhage (SAH) until proven otherwise
Causes of thunderclap headache
Subarachnoid heamorrhage (approx 15% of thunderclap headache)
Intracerebral haemorrhage
Arterial dissection (vertebral or carotid)
Cerebral venous sinus thrombosis
Bacterial meningitis
Rare - spontaneous intracranial hypotension, pituitary apoplexy
Primary headaches (e.g. migraine, exertional headache, cluster headaches) - diagnosis of exclusion
Investigation of thunderclap headache
RxF for SAH
Primary aim is to identify SAH
Urgent CT brain - blood visible in >905% of SAH within first 4 hours
Bloods - U&E, LFT, glucose, FBC, coagulation screen, CRP
Lumbar puncture - performed after 12 hours to look for xanthochromia
12-lead ECG
RxF:
Modifiable: smoking, hypertension and alcohol excess
Non-modifiable - previous SAH, PCKD, connective tissue disease (e.g. Ehler’s Danlos, Marfans syndrome), arteriovenous malformations, FHx
Changes in intracranial pressure
ICP normal level = 7-15mmHg
Monroe-kelie doctrine: Any increase in one component results in reduction of other two
Above 25mmHg small increases in component volume can cause marked raising ICP
Why is raised ICP a problem?
CPP is the net pressure gradient causing blood to flow into the brain
CPP = mean arterial pressure - ICP
Global brain perfusion is reduced when ICP is elevated
Cerebral metabolism is reduced
Raised ICP headaches - history
Worse on lying flat, improved on sitting/standing up
worse in the morning
Persistent nausea/vomiting
Worse on valsalva (coughing, laughing, straining)
Worse with physical exertion
Transient visual obscurations with change in posture
Raised ICP headache - examination findings
Optic disc swelling - papilloedema impaired visual acuity/colour vision Restricted visual fields/enlarged blind spot IIIrd nerve palsy VIth nerve palsy (false localising sign) Focal neurological signs
Causes of raised ICP headaches
MAss effect - tumour, infarction with oedmea, subdural/extradural/intracerebral haematoms, abscess
Inc. venous pressure - cerberal venous isnus thrombosis, obstruction of jugular venous system
Obstruction to CSF flow/absorption - hydropcephalus, meningitis
Idiopathic - idiopathic intracranial hypertension
Low CSF pressure headache - features
Headache worse on sitting/standing up and relieved by lying down
Results from CSF leakage
Low CSF pressure headache - causes
Post-lumbar puncture - 90% develop within 3 days, most resolve spontaneously
Spontaneous intracranial hypotension - results from spontaneous dural tear; Can occur following valsalva
Definition of a stroke
Central nervous system infarction (which includes brain, spinal cord and retinal cells attributable to ischaemia), based on objective evidence of focal ischaemic injury in a defined vascular distribution or clinical evidence of the former with other aetiologies excluded
Outline the pathophysiological processes that can result in stroke
An ischaemic stroke occurs due to a blockage of blood vessels, resulting in reduced blood flow to affected area.
Pathophysiology:
Embolism - Cardiac causes (AF, MI, patent foramen ovale); Aortic Atherome or dissection
Thrombosis - large vessels disease (atherosclerosis); Small vessel disease (Lipohyalinosis or athersclerosis)
Neurotoxicity - Glutamate release due to energy failure causes release of calcium which in turn causes mitochondrial damage (apoptosis) and enzyme induction, resulting in free radicals and DNA damage, leukocyte infiltration etc.
A haemorrhagic stoke occurs due to a ruptured blood vessels, causing leakage of blood and therefore decreased deliverance:
Can identify blood on CT scan - white due to presence of calcium
Cause - hypertension, tumour, burst aneurysm, AVM, head injury and age.
2 subtypes:
○ Intracerebral haemorrhage = bleeding within the brain itself secondary to a ruptured blood vessel –> not caused by trauma
§ Intraparenchymal = bleeding within the brain tissue
§ Intraventricular = bleeding within ventricles
○ SAH = bleeding that occurs outside of brian tissue, between pia mater and arachnoid mater
Investigation/management for acute stroke
Blood tests - U&Es, FBC, ESR, glucose, coagulation screen, creatinine, lipids
Cardiac measure - Echo (AF, recent MI, new onset murmur to assess for atrial or mural thrombus formation)
ECG - may reveal AF
Imaging:
CT - 1st line - essential to exclude haemorrhage and major established infarction to aid in decision regarding re-perfusion therapies
CT angiogram - Contrast injected via peripheral IV catheter to highlight arterial vasculature and detect arterial occlusion - required if thrombectomy being considered
MRI - SIGN guidelines indicate it is useful if patient can tolerate it, particular in minor stroke which may not be detected by CT
Definition of ischaemic stroke
An episode of neurological dysfunction caused by focal cerebral, spinal , or retinal infarction
Definitions of coma
Inability to obey commands, speak & open eyes to pain
GCS 7-8) (?
Classification of stroke
1) Total Anterior Circulation Syndrome (TACS) - Hemiparesis + higher cortical dysfunction and hemianopia. Usually proximal MCA or ICA occlusion
2) Partial Anterior Circulation Syndrome (PACS) - Isolated higher cortical dysfunction OR any 2 of hemiparesis, higher critical dysfunction, hemianopia. Usually branch of MCA occlusion.
3) Posterior Circulation Syndrome (POCS0 - Isolated heminopia OR Brainstem syndrome. Can include perforating arteries, PCA or cerebellar arteries.
4) Lacunar Syndrome (LACS) - Pure motor stroke OR pure sensory stroke OR sensorimotor stroke OR ataxic hemiparesis OR clumsy hand-dysarthria. Perforating artery/small vessel disease.
Defintion of intracerebral haemorrhage
A focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma.
Definition of stroke caused by intracerebral haemorrhage
Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma
Causes of intracranial bleed
Trauma Small vessel disease (deep perforating vasculopathy) Amyloid angiopathy Abnormalities in blood vessels Blood clotting deficiencies Haemorrhagic transformation fo an infarct Tumours Drug usersL cocaine, amphetamine
Treatment of ischaemic stroke
MOA of alteplase
Ischaemic stroke:
1) IV thrombolysis (within 4.5 hours) = with alteplase 0.9mg/kg over 1 hour
2) Thrombectomy (within 6-8 hours after sympotms onset) +/- IV thrombolysis
3) Aspirin (antiplatelet - cannot be given until 24hr screen done)
4) Stroke Unit
5) Hemocranectomy
MOA of alteplase:
It is a recombinant tissue plasminogen activator (rTPA)
MOA - catalyses conversion of plasminogenn to plasmin, which will promote fibrin clot lysis.
SE - Bleeding, allergic reaction
Prevention:
Aspirin will reduce risk of secondary stroke, MI or vascular death. Dipyridamole further reduces so usually given with aspirin.
Statins
Warfarin and Direct anticoagulatns (DOACs) especially reduce risk in AF
Smoking cessation
Treatment of intracerebral blood (haemorrhagic stroke)
Intracerebral bleed (Haemorrhagic stroke):
Blood pressure control
Stroke Unit
Neurosurgical evacuation
Common secondary prevention for of stroke
Antiplatelet - Aspirin or clopidogrel. No antiplatelet therapy for at least 24 hours after thrombolysis and a CT must be performed first to confirm there is no haemorrhage.
Ideally prescribe clopidogral 75mg once daily
Modified-release dipyridamole in combination with aspirin considered if patient intolerant to clopidogrel
In cases of AF: Stop antiplatelet therapy Commence anti-cagulation Non-valvular AF - DOAC or warfarin Valvular AF - warfarin
Antihypertensives:
BP lowered below 140/85mmHg
Statins:
Atorvastatin or simvastatin
Rehabilitation: Speech and occupational therapy Physiotherapy Smoking cessation Dietician and exercise regime Driving restrictions
Describe the incidence and prevalence of MS in Scotland/UK
Define MS
What causes MS?
Scotland has the highest incidence and prevalence in the world
Definition: MS is an idiopathic inflammatory demyelinating disease of CNS
Genetic factors
Sunlight/vit D exposure
Viral trigger - possibly EBV
Multifactorial - smoking is a major risk factor
Symptoms that may develop into MS:
Optic neuritis, clinically isolated syndromes, transverse myelitis, radiologically isolated syndromes (MRI scan performed in patients who does not hvae symptoms or signs of MS but there is an incidental finding of MS)
Describe the characteristic appearance and immunopathology of demyelinating lesions within the central nervous system
Features of transverse myelitis
Clinically isolated syndromes (that can cause MS)
Demyelination results in loss of neurological function - weak leg, visual loss, urinary incontinence
These deficits usually develop gradually, last more than 24 hours and may gradually improve over days to weeks
Hidden relapses - optic neuritis, bells palsy, labyrinthitis, sensory symptoms, bladder symptoms in young man/women without children
Transverse myelitis:
Inflammation of the spinal cord
Weakness, sensory loss, incontinence
Many causes other than MS (e.g. HIV)
Clinically isolated syndromes:
Single episode of neurological disability due to focal CNS inflammation.
Can include optic neuritis and transverse myelitis
May be a first attack of MS
Can happen after infection and not be related to MS
Discuss clinical presentation and diagnosis of MS
Features of optic neuritis
Central - fatigue, cognitive impairment, depression, unstable mood
Visual - nystagmus, optic neuritis, diplopia
Speech - dysarthria
Thorat - dysphagia
MSK - weakness, spasms, ataxia
Sensation - pain, hypoesthesias, paraesthesias
Bowel - incontinence - Diarrhoea or constipation
Urinary - incontinence - frequency or retention
Diagnosis of MS:
Is diagnosed when there is evidence of 2 or more evidence of demylination disseminated in space and time
Optic neuritis:
Painful visual loss that comes on over a few days
May resolve after a few weeks
Risk of developing into MS depends on MRI scan and oligoclonal bands
Outline the role of investigations in the diagnosis of MS
MRI brain and cervical spine with gadolinium contrast can diagnose if evidence of demyelination in 2 regions. - ate dissemination in time)
Can be done with one scan i.e. evidence of demyleination in 2 regions can indicate dissemination in space; If enhancing and non-enhancing areas of demyelination are seen this can indicate dissemintation in time.
LP - CSF olgioclonal bands (require matched blood sample) - immunoglobulin bands suggesting inflammatory response, suggests MS if only in CSF. CSF - cell counts, glucose and protein
Bloods (e.g. B12/folate, Serum ACE, lyme serology, ESR/CRP, ANA/ANCA/RF, Aquaporin-4 antibodies (if transverse myelitis//optic neuritis)are done to exclude any other possible cause of symptoms
CXR done to exclude sarcoidosis
Visual evoked potentials
What are oligoclonal bands?
Immunological bands seen in blood and spinal fluid after protein electrophoresis.
Function of visual evoked potentials
Measure conduction of nerve signals in optic nerve to look for subclinical optic neuritis
Conduction will be slower if a patient has had optic neuritis in the past.
Relapse vs Pseudo-relapse (MS)
A relapse usually involves a new neurological deficit that lasts for more than 24 hours in the absence of pyrexia or infection. Not all require treatment but steroid
A pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old area of demyelination in the context of heart or infection
If evidence of infection this should be treated.
Treatment of MS relapse
Not all relapses need treatment
Steroids may speed up recovery from relapse but will not effect progression of diease.
Steroids should not be given if any evidence of infection.
Should get physiotherapy +/- occupational therapy
May organise MRI with contrast to look for active disease and change treatment.
1g of IV methylprednisolone for 3 days or 500mg oral methylprednisolone for 5 days AND PPI for gastroprotectiion
Ideally prescribe at 9AM to avoid sleep disturbance
…
Primary vs secondary progressive MS
Primary - at least 1 year of disease progression with diagnosis supported by CT and olgioclonal bands. Treat symptoms or use Ocrelizumab
Secondary - RRMS in past but now progressive disease without relapse of inflammation on scan.
Treat potentially using Siponimod
Understand the treatment options for Ms (not an ILO?)
Powerful drugs:
Alemtuzumab - 2 short courses over a year, then further treatment if needed; high risk of secondary autoimmune problems (thyroid, ITP, Goodpastures); May improve diasbility.
Natalizumab - Monthly infusions; VEry effective treatment for rela[pses; Serious risk of fatal progressive Multifocal Leukoencephalopathy if infected with JC virus
Oral treatments:
Fingolimod: Daily tablet; Less effective than the above drugs; Risk of infections; May slow heart rate
Dimethyl Fumurate: Twice daily tablet; Less effective Fingolimod; Low white cell counts; Risk of infections
Provide overview of pathological process in common dementia
Dementia is the development of multiple cognitive deficits - The cognitive or behavioural impairment involves a minimum of two of the following domains:
- memory
- Executive function
- Language
- Apraxia/Visuospatial
Dementia is slowly progressive over years - at later stages all manifests similarly
Severe, acquired and must involve more than one brain region
Describe clinical presentation of common dementias
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Briefly discuss investigation of common dementia syndromes
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Recap types of memory
Declarative (explicit):
Episodic - times, places, emotions. Localised - mesial temporal lobe and hippocampus.
Semantic - facts, knowledge. Widely distributed.
Working - core executive function, decisions etc. Distributed - frontal lobes for attention, temporal and parietal
Describe pathogenesis and clinical presentation fo SAH
A SAH is an acute cerebrovascular event, with possible devastating effects on CNS (e.g. stroke) and profound impact on other organs too.
Common in those with degenerated blood vessels, most common age 40-60.
Predisposing Rx factors - smoking, female, hypertension, positive family hisotry, ADPCL, Ehler’s Danlos, Coarctatoin of aorta
Aneursym formation (although 15-20% are non-aneurysmal):
Extensive inflammatory and immunological reactions are common in unruptured intracranial aneurysms and may be related to formation and rupture.
Causes cerebral bleeding:
- Cerebral arteries - cause subarachnoid bleeding
- Arteries which penetrate brain tissue - intracerebral bleeding
Common cause of SAH:
- Trauma
- Aneurysm
- Tumour
- Arterious venous malformation
- anticoagulanta
Typical history for SAH
Thunderclap headache
Loss of consciousness, seizures, visual, speech and limb disturbances
Sentinel headache precedes SAH - sudden, intense and persistent
Clinical examination findings for SAH
Photophobia Meningism Subhyaloid haemorrhages Vitreou haemorrhages - Terson's syndrome Speech and limb disturbances Pulmonary oedema
Grading of SAH
Grade I - GCS 15 Grade II - GCS 13-14 without deficit Grade III - GCS 13-14 with deficit Grade IV - GCS 7-12 Grade V - GCS 3-6
Investigations for SAH
CT will confirm the diagnosis and gives clue to cause - also identifies complications and gives prognostic marker through Fisher Grade, predicting risk of cerebral vasospams
LP - Xanthochromia is yellowing of CSF (bilirubin vs oxyhaemoglobin)
CT angiography/MR angiography
Hyponatraemia - cerebral salt wasting with leaking of salt and water
ECG or echo (tako tsubo cardiomyopathy) changes
Elevated troponin levels often seen few days after
Management and treatment of SAH
Management: Bed rest Fluids - 2.5-3l normal saline Anti-embolic stockings Nimodipine Analgesia Doppler studies
Treatment:
Surgical clipping of aneurysm to prevent further pressure from blood
Endovascular treatment - coils, stent, glue
Conservative
Outline the complications of SAH
Re-haemorrhage occurs mostly immediately after initial bleed, with higher risk in poorly graded patients. Risk can be reduced with immediate aneurysmal repair.
Delayed ischaemia occurs 3-10 days after, presenting with progressive deterioration in LoC associated with new deficit. Treatment involves: fluid management, nimodipine, inotropes, angioplasty - balloon angioplasty
Hydrocephalus can be treated with a shunt, LP or with extra ventricular drain
Hyponatraemia can be treated with hypertonic saline and fludrocortisone
Cardiopulmonary complications arise dur to sympathetic and catecholamine release - can lead to myocardial injury such as LVF (Tako-tsubo cardiomyopathy), arrhtymias, PEs, LRTIs
UTIs and seizures also increased risk
What are the 3 subscales for GCS
Eye opening: 4 - Spontaneous 3 - To verbal command 2 - To pain 1 - None
Verbal response (adapted with 'T' if intubated): 5 - Orientated (Time, Place, Person) 4 - Confused 3 - Inappropriate 2 - Incomprehensible sounds 1 - None
Motor response: 6 - Obeys commands 5 - Localizes pain 4 - Normal flexion 3 - Abnormal flexion 2 - Extension - arms out and hands turned 1 - None
Anatomy of the brain
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Outline causes for loss of consciousness
Seizure
Syncope
Non-epileptic attacks
Rarer causes: Migraine Narcolepsy/cataplexy Transient Global Amnesia Panic attacks
Define seizures and epilepsy
Epilepsy = at least 2 unprovoked episodes of seizure
Seizure - episode of neuronal hyperactivity which is associated with symptoms, most common in children and >50
Briefly outline different types of seizure
Generalise - has no focal area so therefore spreads out.
Causes tonic continuous seizures as mroe of an area is reach through the hyperactivity.
Usually has 60 second duration followed by deep sleep
Common features: Photosensitivity (triggered by trees, lights, tunnel etc.); Age (9-26 y/o affected); Triggers e.g. alcohol, stress, periods or sleep deprivation; Family history of IGE; Myoclonus (especially in the morning); Lack of aura; Seizures within 2 hours of wakening; Abnormal EEG.
Respiratory muscles cannot contract so may cause choking
Focal - are localised to one point so spread of hyperactivity is limited. Originates within networks linked to one hemisphere. May then spread to both hemispheres.
Common features:
History of trauma/birth trauma; Focal aura/sequelae; Post-attack confusion or drowsiness; Automatisms (lip smacking); Nocturnal events.
If no impact of awareness - simple partial seizure
If awareness impaired - complex partial seizure
Differential diagnosis of seizure
Diagnosis of seizures
Differential diagnosis of seizure:
Syncope, NEAD (non-epileptic attack disorder), migraine, narcolepsy, transient global amnesia, panic attacks, MI, shock, head trauma
Clinical history is important - obtain from patient AND one eye-witness soource
Investigations:
ECG will rule out other diagnoses
Brain imaging is done - MRI
EEG is a brain wave test observing activity of brain when at rest - Test takes 1 hour; Hyperventilation and drowsiness are common; Photic stimulation is used
Investigations for epilepsy
Acute management f a seizure
EEG - hyperactivity - can be caused by normal physiology. Test takes 1 hour. Photic stimulation. ECG - rule out MI, AV block Drug/alcohol screen Routine bloods Lumbar puncture - meningitis MRI
Keep them out of harms way
Put them in recovery position
Record their pulse
If movements stop and no impairment of ABCs, does not need hospitalisation once recovers awareness
Outline longer term management of epilepsy
Focal epilepsy:
Lamotrigine
Carbamazepine
Levetiracetam
Generalised epilepsy:
Valproate
Levetiracetam
Lamotrigine
Definition of Status epilepticus
+ management of status epilepticus
This is >2 seizures without full recovery or neurologic function between seizures OR continuous seizure activity for more than 30 minutes
- Effectively repetitive OR prolonged epileptic seizures
Management:
Check for ongoing provocation
Glucose, infection, metabolic panel, U&E, ABG, CT, Toxicology screen
IV benzodiazapines and IV phenytoin
Intubate, sedate, consider ICU escalation
Describe examples of what clinical signs might be seen with lesions of the frontal lobe in cerebral hemisphere
Sudden and dramatic change in personality - loss of social awareness, disinhibition, emotional instability, irritability or impulsiveness
Describe examples of what clinical signs might be seen with lesions of the parietal lobe in cerebral hemisphere
Contralateral hemisensory loss Asereognosis - unable to identify 3D shape by touch Agraphaethesia Contralateral homonymous lower quadranaopia Sesnory seizures Dysphasia/aphasia Dyslexia Apraxia
Describe examples of what clinical signs might be seen with lesions of the temporal lobe in cerebral hemisphere
Disturbance of auditory sensation and perception
Disorder of visual perception
Disturbance of language comprehension
Describe examples of what clinical signs might be seen with lesions of the occipital lobe in cerebral hemisphere
Homonymous loss of vision if one-sided
Hallucinations and illusion
Describe examples of what clinical signs might be seen with lesions of visual pathway
Monocular vision loss Bitemporal heminopia Contralateral homonymous heminopia Contralateral superior quadrantanopia Contralateral inferior quadrantanopia Contralateral homonymous quadrantanopia
Describe examples of what clinical signs might be seen with lesions of the diencephalon
Failure to trhive Vomiting Hyperkinesia Low blood sugar Hyperactivity Tremor Sweating Amnesia
Describe examples of what clinical signs might be seen with lesions of the cauda equina
Neurological symptoms in lower body Bladder or bowel incontinence Sharp or stabbing pain in legs or lower extremities Localised LBP Saddle anaesthesia
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Epidemiology of Parkinsons Disease
Common neurodegenerative disorder (2nd most common after AD)
Primarily a sporadic disorder
Affects men more than women
Aetiology of PD
Primarily a sporadic disorder
Many genes contribute to development of PD - LRRK2 gene mutation is the most common
Pathology of PD
Loss of dopaminergic neurones within substantia nigra, contributing to the loss of dpamine production
The surviving neurones contain Lewy bodies due to oxidative stress, mitochondrial failure, protein aggregation, interference with DNA transcription etc. The se contain alpha-synuclein or ubiquitin.
PD manifetss clinically after loss of approx 50% of dopaminergic neurones.
Pathological progression is set in stages, with clinical manifestation determined by level of Lewy bodies:
Stage 1-2: Lewy bodies in medulla/pons and olfactory nucleus. Pre-symptomatic or pre-motor e.g. loss of smell
Stage 3-4: Lewy bodies in midbrain - substantia nigra and pars compacta. Parkinsonism only becomes evident after extensive nigral damage.
Stage 5-6: Lewy bodies in neocortex. Development of PD dementia
Suggested mechanisms for Lewy body formation
Oxidative stress Mitochondrial failure Excitotoxicity Protein aggregation Interference with DNA transcription Nitric oxide Inflammation Apoptosis Trophin deficiency Infection
Clinical features of PD
Bradykinesia - slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions. - Shuffling gait
With at least one:
Muscular rigidity - increased tone
Slight resting tremor
Postural instability - loss of reflexes that keep you upright
Asymmetric disorder - starts and remains worse on one side
Non-motor symptoms:
Neuropschiatric - dementia, depression, anxiety
Autonomic - constipation, urinary urgency/nocturia, erectile dysfunction, excessive salivation/sweating, postural hypotension
Sleep - rem sleep behaviour disorder, restless legs
other - reduced smell, fatigue, pain and sensory symptoms
Differential diagnosis of PD
Benign tremor disorders Dementia with Lewy bodies Vascular parkinsonism Drug-induced parkinsonism - chronic use of dopamine agonists Toxins
Investigations for PD
Bloods to determine other possible causes of tremor - thyroid or Wilson’s
Structural imaging - CT/MRI should be normal; Abnormal in vascular parkinsonism
Functional imaging - imaging of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative parkinsonism
Outline the principles of management of Parkinson’s disease
Levodopa:
This is taken up by dopaminergic neurones and decarboxylated to dopamine within presynaptic terminals.
Prescribed alongside a dopa-decarboxylase inhibitor:
L-DOPA + Carbidopa –> Sinemet
L-DOPA + Benserazide –> Madopar
Half life approx 90 mins
Dosing 200-1000mcg/day
Side effects:
Peripheral - nausea, vomiting, postural hypotension
Central - confusion, hallucinations
Long-term - motor complications after 5 years of treatment (dyskinesia)
Dopamine agonists (e.g. Ropinirole, Pramipexole, Rotigotine, Apomorphine
These act directly on post-synaptic striatal dopamine receptors (D2 subtype)
Longer half life but less effacious than L-DOPA.
Side effects:
Dopaminergic side effects, somnolence, impulse control disorders (hypersexuality etc.), nightmares
MAO-Beta Inhibitors - Selegilline, Rasagiline:
These prevent dopamine breakdown by binding irreversibilty to monoamine oxidase
Well tolerated by patients
COMT-inhibiotrs - Entacapone, Tolcapone:
These inhibit Catechol-O-methyltransferase in order to increase half-life/duration of action of LDOPA
Co-prescribed with L-dopa in later disease
Side effects:
Dopaminergic effects, diarrhoea
Problems in advanced PD
Motor:
Motor complications - ‘On/Off’ fluctuations; L-dopa induced dyskinesia
Poor balance/falls
Speech/swallowing disturbance
Cognitive - Dementia
Understand methods of surgical intervention for PD
Deep brain stimulation of Subthalamic Nucleus can be used in advanced disease:
2 electrodes surgically attached to subthalamic nucleus (close to substantis nigra) and to a pace-maker to stimulate when required
Need to be younger than 70 and have to have responded well to Levodopa
Describe the role of MDT in management of PD
GP Neurologist/care of elderly physician PD nurse specialist Physio, speech and language, and occupational therapists Psychiatrist and psychologist
Degenerative causes of PD
Dementia with Lewy bodies
Progressive supranuclear palsy
Multiple system atrophy
Corticobasal degeneration
Secondary causes of PD
Drug induced - chronic use of dopamine antagonists
Cerebrovascular disease
Toxins (e.g. carbon monoxide, organophosphates, MPTP)
Post-infection
Aetiology of CNS infections (primary infections)
Bacterial (e.g. meningococcus, Pneumococcus, HI, Listeria, TB) - causes Meningitis, Meningo-encephalitis, Abscess
Viral (e.g. HSV, VZV, Enterovirus, HIV, Mumps) - causes Encephalitis, Meningitis
Fungal (e.g. Cryptococcosis) - causes Meningo-encephalitis, Mass lesion
Protozoal (e.g. Toxoplasmosis) - causes Mass lesion, Eosinophilic-meningitis
What is the most common cause of viral meningitis
Enterovirus infection
Signs and symptoms of meningitis
95% will have 2 of: Headache, neck stiffness/rigidity, reduced GCS or fever (neck stiffness/rigidity only 50%).
Confusion indicative of cerebritis/encephalitis
Rash - purpuric and/or petechial rash (but macular rash is seen early on, especially in meningococcal)
Types of secondary CNS infection
Secondary CNS infections is a systemic infection with secondary infection of the CNS
- Endocarditis which can cause cerebral abscess or meningitis
- Sequestrated parasites in falciform malaria
Aetiology of Bacterial meningitis
Risk factors:
Travel (e.g. to Africa), Alcohol and chronic liver disease, Cochlear implant, IVDUs - Strep and Staph infection, Pig handlers - Strep Suis
Pneumococcal is most common cause:
70% have underlying disorder e.g. middle ear disease, head injury (CSF leak), neurosurgery, alcohol, immunosuppression (HIV)
Listeria: More commonly seen in pregnant or immunosuppressed patients
Features of pneumococcal meningitis
Neurology - focal signs, seizures, VIII nerve palsy (–> hearing problems)
Other signs of pneumococcal infection: CAP, ENT, Endocarditis
Can loose whole limbs from pneumococcal meningitis - due to vasculitis
What are the prognostic indicators for bacterial meningitis (signs of a poorer outcome)?
Pneumococcus Reduced GCS CNS signs Older age (>60 years) CN palsy (pneumococcal) Bleeding (meningococcal)
Investigations for suspected Meningitis
History and exam - examine throat (strep throat?) and cervical lymph nodes
Blood cultures - FBC, U&Es, LFTs, CRP, PCR (get raised WCC, raised CRP,
Throat culture, Viral gargle
Lumbar puncture - cell count, gram stain, culture and PCR, protein and glucose, viral PCR (often raised protein and low glucose)
CT scan done before LP if:
GCS <= 12, CNS signs, Papilloedmea, immunocompromised, Seizure
CT excludes mass lesion, gross cerebral oedema but doesn’t exclude RICP (raised ICP)
Antibiotics need to be given BEFORE CT scan
When is a LP contraindication, when investigating for meningitis?
Brain shift, rapid GCS reduction, Res/cardiac compromise, Severe sepsis, Rapidly evolving rash, Infection at LP site, Coagulopathy
What Tx should you give for suspected bacterial meningitis
IV cefriaxone 2g 12hrly
Or if penicillin allergy - IV Chloramphenicol 25mg/kg 6 hrly
If >=60, immunocompromised, pregnant, alcohol excess, liver disease or if listeria meningitis is expected ADD IV amoxycillin 2g 4hrly to ceftriaxone
If bacterial meningitis strongly suspected add IV dexamethasone and to refer to ID
Definitive antibiotic therapy for BM - meningococcal, pneumococcal and listeria
Meningococcal:
IV ceftriaxone or benzyl penicillin
5 days
Pneumococcal:
IV Ceftriaxone or Benzyl Peniciilin
10-14 days (increase duration if complications)
Listeria:
IV Amoxicillin (Stop Ceftriaxone)
21 days
If strong suspicion of BM suspected add IV dexamethasone 10mg 6 hrly (for 4 days)
Features of viral meningitis
Usually diagnosed only after exclusion of BM
No confusion:
Most common cause is Enterovirus> HSV2> VZV> HSV1> HIV> Mumps
Features of intra-cerebral TB
Sub-acute (weeks) CN lesions usually involve III, IV, VI, IX CSF may be normal Treat with steroids Also administer RIPE: Rimfampicin Isoniazid Pyrazinamide Ethambutamol
Features of viral encephalitis
Presents with confusion, fever +/- seizures
Diagnosed through lymphocytic CSF (normal glucose), EEG (temporal lobe spikes), MRI (inflammatory changes in temporal lobe) and +ve PCR
Commonest cause of viral encephalitis = HSV
Treatment:
IV Aciclovir for 2-3 weeks (if HSV or VSV) - no Tx for enterovirus or mumps
HIV brain disease - features
Consequence of unrecognised/untreated infection and marker immunodeficiency or life-style:
Encephalitis (ARVs)
Dementia
Neuro-syphilis (secondary or tertiary)
Opportunistic (TB, Cryptococcus, Toxoplasmosis, JCV)
Features of Progressive focal Multifocal Leucoencephalopathy (PMLE)
This is progressive motor dysfunction
Common in immunocompromised and post-renal transplant
Caused by JC virus
No treatment, but ARVs given if HIV pos
Features of Crytococcal meningitis
Underlying immunodeficiency (e.g. HIV)
Presents with CN VI and VII palsy, scarring of head
Results in raised ICP due to increased CSF - drain this away
Treat with Amphotericin B and Flucytosine or Fluconazole
FEatures of Intra-Cerberal Toxoplasmosis
Caused through toxoplasma gondii
Presents with headache, seizures and focal CNS signs
Common in immunocompromised, HIV - we all carry organism but suppressed
Treated through Sulphadiazine and Pyramethamine
DASPITE of SAH
D - High intesnity headache that reaches maximal intensity <5 mins after onset and is linked to bleeding into the subarachnoid space
A - Trauma, ruptured saccular or berry aneurysm
S+S - Sudden onset thunderclap headache, seizure, visual disturbance, stiff neck, Terson’s syndrome, photophobia
Pathophysiology - Blood extravating into subarachnoid space, commonly aneurysms located in anterior cerebral circulation
I - Non-contrast CT, LP, routine bloods
T - Nimodipine, analgesia, fluid resus, coiling or clipping
E - post-menopausal women, connective tissue disorders, smoker, FHx, HTN, previous SAH, polycystic kidney disease
Features of TIA
TIA = Transient Ischaemic attack = Symptoms mimicking a stroke that will appear and last <24 hours
- 40% of people who have a TIA will have a stroke
- Nearly half of all strokes occur within days after TIA
- Crescendo TIAs = 2 or more TIA within 1 week = Urgent admission for Ix and Mx
- Cause:
○ Atherothromboembolism from carotid
○ Other embolism or thrombus
- Anyone with continuing neurological signs after 1st assessment = assume stroke
- Ix - carotid imaging within 1 week of onset of symptoms
- Rx - those with carotid stenosis require a carotid endartectomy or stenting, lifestyle modifications
Features of intra- cerebral TB
Subacute (weeks) CN lesions usual (III, IV, VI, IX) CSF may be normal Give steroids Paradoxical worsening is usual
