Neurology Flashcards
Functional division of the pyramidal tracts?
What are pyramidal tracts responsible for?
Corticospinal tracts-lateral and anterior
Corticobulbar tracts
Responsible for voluntary control of musculature of body and face
Structure of corticospinal tracts/what path do they follow?
Originate at cerebral cortex and pass through medulla oblongata
- Lateral corticospinal tract (90%) decussate at medulla and terminate in the ventral horn (at all segmental levels)
- Anterior tract remains ipsilateral and decussates/terminates in cervical/upper thoracic segmental levels
What do the extrapyramidal tracts do?
What tracts are there?
Where do they originate, and which decussate?
Involuntary and autonomic control of all musculature eg muscle tone, balance, posture, locomotion
All originate at the brainstem
Vestibulospinal and reticulospinal don’t decussate
Rubrospinal and tectospinal decussate
How many pairs of spinal nerves are there?
31
8C, 12T, 5L, 5S, 1C
What would examination of an UMN lesion show?
Normal muscle bulk, increased tone, decreased strength, no fasciculations, hyperreflexia (brisk)
What would examination of a LMN lesion show?
Decreased bulk/wasting, normal or decreased tone, decreased strength, may have fasciculations, decreased or absent reflexes
Name peripheral neuropathies (polyneuropathy) that are predominantly motor loss
Guillain barre syndrome (GBS), chronic inflammatory demyelinating neuropathy (CIDP ie chronic version of GBS), hereditary sensiromotor neuropathies (HSMN eg Charcot-Marie-Tooth disease), diphtheria, porphyria
Name peripheral neuropathies (polyneuropathy) that are predominantly sensory loss
Deficiency states eg B12/folate, diabetes, alcohol/toxins/drugs, leprosy, amyloidosis, metabolic abnormalities eg uraemia
Defining features of polyneuropathy?
Usually chronic and slowly progressive, starts in legs and longer nerves, can be sensory/motor/both
What is mononeuritis multiplex?
Painful, asymmetrical, sensory and motor neuropathy, subacute presentation.
Inflammatory/immune mediated.
Common causes=vasculitides eg Churg Strauss and connective tissue disorders eg sarcoid
Name 2 common mononeuropathies
Carpal tunnel syndrome-median nerve compression in flexor retinaculum
Common peroneal nerve in the leg
Ulnar nerve at the elbow
Radial nerve in the axilla
What investigations are involved in a neuropathy screen?
FBC, ESR, U+E, glucose, TFT, CRP, serum electrophoresis, B12 and folate, anti gliadin, (TPHA and HIV)
What investigations are involved in a vasculitic screen?
FBC, ESR, U+E, Cr, CRP, ANA, ANCA, anti dsDNA, RhF, complement, cryoglobulins
Principles of treatment of inflammatory neuropathy?
And vasculitic neuropathy?
Inflammatory eg CIDP: prednisolone with steroid sparing agent such as azathioprine
Vasculitic eg with Wegners: prednisolone with immunosuppressant such as cyclophosphamide
How does GBS arise?
What is it?
Autoimmune response leading to demyelination
Post infectious- respiratory or GI (campylobacter)
Subacute (<6 weeks), ascending paralysis/numbness/areflexia
What will you see on LP with GBS?
Raised CSF protein
How to manage GBS?
Treat with IV Ig or plasmapheresis Supportive Monitor FVC Consider ITU review Recovery may take weeks to years
What is Myasthenia Gravis?
Autoimmune disorder with antibodies against nicotinic ACh receptors
Commonly due to thymus dysfunction- hyperplasia and thymomas
Results in generalised and fatiguable weakness
Different potential presentations of MG?
Proximal limbs, neck and face (head drop and ptosis), extraocular (complex diplopia), bulbar (speech and swallow issues especially in elderly), ocular (seen in 10-25%)
NB/ at risk of other AI diseases
How to investigate for MG?
Tensilon test used in the past
Look for AChR antibodies
EMG-looking at NMJ
CT thorax (breathing)
How to treat MG?
Acetycholinesterase inhibitors eg pyridostigmine
Immunosuppressants- steroids started slowly, azathioprine/methotrexate/mycophenolate
Thymectomy if indicated
What is a myasthenic crisis?
Severe weakness including respiratory muscles-high risk of death
Caused by infection/natural disease cycle/under or overdose of medication
Urgent reviews by anaesthetists and neurologists needed
What is MND? UMN or LMN? How to diagnose? What is spared? Survival?
Degeneration of motor neurons in motor cortex and anterior horns of spinal cord. Asymmetric weakness. Bulbar or limb onset.
UMN and LMN signs
LP/EMG/MRI to rule out, mainly a clinical diagnosis
No sensory, visual or bladder/bowel involvement
Usually 2-5 years survival
Name 2 common muscle disorders
Steroid myopathy, statin myopathy, metabolic and endocrine myopathies, myotonic dystrophy
Name 2 uncommon muscle disorders
Duchenne and Becker + most muscular dystrophies eg FSHD (facioscapulohumeral muscular dystrophy)
Inflammatory muscle disease eg polymyositis
Mitochondrial disorders
What is the WHO definition of a stroke?
Clinical syndrome consisting of rapidly developing clinical signs of focal disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other than a vascular origin
What are the common symptoms of a carotid territory stroke?
Weakness of face, leg, arm, amaurosis fugax, impaired language
What are the common symptoms of a posterior circulation stroke?
Dysarthria, dysphasia, diplopia, dizziness, ataxia, diplegia
Proportion division of types of stroke?
Ischaemic- around 85%
Haemorrhagic- around 15%
What is the Oxford stroke (Bamford) classification of stroke?
Total anterior circulation stroke
Partial anterior circulation stroke
Lacunar syndrome
Posterior circulation syndrome
How to differentiate TACS from PACS (Bamford)?
TACS has all 3 of; unilateral weakness, homonymous hemianopia and higher cerebral dysfunction
PACS has just 2 out of 3
How to identify Lacunar syndrome (Bamford)?
One of following: pure sensory stroke, pure motor stroke, sensori-motor stroke, ataxic hemiparesis
How to indentify posterior circulation syndrome (Bamford)?
One of the following:
CN palsy and a contralat motor/sensory deficit
Bilat motor/sensory deficit
Conjugate eye movement disorder eg gaze palsy
Cerebellar dysfunction eg ataxia/nystagmus/vertigo
Isolated homonymous hemianopia or cortical blindness
Potential signs of an anterior circulation infarction
Which arteries is this?
Arteries=middle and anterior cerebral arteries
Contralateral weakness, contralateral sensory loss/inattention, dysarthria, dysphasia (receptive/expressive), homonymous hemianopia/visual inattention, higher cortical dysfunction
What is the underlying pathology of a lacunar stroke?
Occlusion of deep penetrating arteries. Affects small volume of subcortical white matter.
Small vessel disease-arterial wall disorganisation, microatheroma, lipohyalinosis
General flow diagram of how to manage a stroke
think FAST/recognition
ABCDE, bloods. Brief history and exam, BP, NIHSS
Urgent CT head +/- CTA
Thrombolysis +/- mechanical thrombectomy or aspirin
Investigate cause, screen and prevent complications, secondary prevention, rehab
When can you give thrombolysis? What with?
IV administration of tissue plasminogen activator eg alteplase
Within 4.5 hours of symptom onset (or time they were last seen well)
Name 4 CIs to thrombolysis
Suspect SAH, active bleeding, symptoms only minor or rapidly improving, low platelets, recent heparin treatment, recent warfarin treatment and INR elevation, recent post MI pericarditis, recent LP, BP over 185/110 consistently, BG <3 or >20, pregnancy, active pancreatitis
What is involved in post-thrombolysis care?
Aggressive BP monitoring, vigilance for complications, 24 hour CT head (haemorrhagic transformation)
What is mechanical thrombectomy? Time window?
Recanalisation of the culprit vessel
6 hour time window for anterior circulation stroke
Can be used alongside IV thrombolysis, but a limited resource
What investigations are used after the initial management of stroke?
Bloods-FBC, ESR, U+Es, lipids, LFTs, CRP, clotting screen, glucose and HbA1c ECG +/- 72 hour tape Carotid doppler USS Echo MRI
For a young patient/atypical stroke consider HIV and vasculitic screen, thrombophilia screen, homocysteine. Cardiac investigations, vasc imaging eg CTA
Management after stroke investigations?
MDT approach
Lifestyle: smoking/drugs/alcohol cessation, diet modifications, exercise, driving advice
Medical: VTE assessment, hydration, NG feeding+/- PEG, spasticity (physio, botox), monitor for infection
Secondary prevention
Surgical: eg carotid endarterectomy
What is involved in secondary prevention after an ischaemic stroke?
Antiplatelets: 300mg aspirin po/pr for 2 weeks and clopidogrel lifelong
Anticoagulation: if in AF may need to wait for 2 weeks- HASBLED and CHADSVASC scores
Hypertension: target <130/80
Cholesterol: statin, aim for 40% reduction in non-HDL cholesterol
How to manage a haemorrhagic stroke? (drugs and corresponding)
Reversal of any anticoagulation
Warfarin= beriplex and vitamin K
Heparin= protamine
LMWH= potentially reversible with protamine
Apixaban/rivaroxaban/edoxabana=possibly reversible with beriplex
Dabigatran=idarucizumab
Red flags in a headache history
New headache over 60 years, thunderclap, infective symptoms, history of malignancy
Red flags in a history of weakness
Loss of sphincter control, sudden onset, progressive, respiratory or swallowing problems
Red flags in a history of visual disturbance
Any other associated symptom eg headache and visual loss in an older person
Important aspects in a history of speech disturbance
Comprehension (receptive/Wernicke’s dysphasia)
Production (expressive/Broca’s dysphasia)
Repetition (conductive dysphasia, arcuate fasciculus- connecting brocas and wernickes)
Articulation/dysarthria (cerebellar, bulbar, pseudo-bulbar donald duck speech)
Phonation/dysphonia (eg resp muscle weakness)
What are some mechanical and neurological causes of dysphagia?
Mechanical= stricture and achalasia
Neurological= bulbar and pseudo-bulbar palsy, brainstem pathology, MG, MND
Describe the AMT
What are some other cognitive state assessment methods
AMT/abbreviated mental test score:
Tell pt to recall address, age, time, year, recognise two people, DOB, dates of 2nd world war, name of present monarch, name of hospital, count 20 to 1
What do you see in CN3 palsy?
eye looking down and out with ptosis (ipsilateral)
What is internuclear ophthalmoplegia?
Disorder of conjugate lateral gaze. Lesion in medial longitudinal fasciculus.
Ipsilateral to eye that fails to adduct across
Difference between UMN and LMN lesions of facial nerve
UMN lesions spare the forehead
LMN lesions=Bells palsy doesn’t spare the forehead
Rinne’s test- describe the finding
In conductive hearing loss, bone conduction is louder than air conduction
(In sensorineural deafness, air conduction is louder than bone conduction)
Normal=air conduction louder than bone conduction
Weber’s test- describe the finding
In conductive hearing loss, sound is heard louder on side of affected ear
(In sensorineural deafness, sound heard louder of intact ear)
Normal=equally loud
Difference between spasticity and rigidity?
Spasticity=amplitude and velocity dependent- “clasp knife”,affected pyramidal tracts
Rigidity=independent of amplitude and velocity, lead pipe, cogwheel (rigidity an tremor together), affected basal ganglia
How to recognise cerebellar lesion/coordination?
DANISH
Dysdiadokinesis, ataxia, nystagmus, intention tremor, speech, hypotonia
What are considered neurological emergencies?
Coma Sudden or subacute new headache Weakness Visual loss Status epilepticus Other eg acute loss of bladder function, hemiballismu, severe chorea, severe dysphagia
What subtypes of weakness are there, when considering neurological emergencies?
Generalised +/- respiratory failure
Acute/subacute para/quadriplegia
Acute hemi/monoplegia (stroke)
Describe GCS
Glasgow coma score
Eye opening: 1=none, 2=to pain, 3=to voices, 4=spontaneously
Motor response: 1=none, 2=extension to pain, 3=flexion to pain, 4=withdraw from pain, 5=localises to pain, 6=obeys commands
Verbal response: 1=none, 2=groans, 3=inappropriate words, 4=confused speech, 5=orientated
Name 5 common causes of coma
Drugs/toxins (opiates), anoxia, mass lesions (bleeds), infections (HSE, bacterial meningitis), infarcts, metabolic (hypoglycaemia, DKA, hepatic encephalopathy, uraemia), SAH, epilepsy
Name 2 uncommon causes of coma
Mass lesions (tumours), hypothermia, psychiatric, venous sinus occlusions
What is status epilepticus?
Official definition: Persistent seizure activity for 30 mins or more-continuous or intermittent attacks without recovery of consciousness
Practical definition: convulsive seizure activity with loss of consciousness for over 10 mins
What warrants status epilepticus in different seizure types?
Generalised tonic-clonic= 5 mins
Focal=10 mins
Absence=10-15 mins
What are potential consequences of status epilpeticus?
Increased CNS metabolic consumption Mortality Rhabdomyolysis Renal failure Metabolic acidosis Hyperthermia Heart and other organ effects
How to manage status epilepticus?
1st line= benzodiazepine eg IV lorazepam/diazepam/clonazepam or rectal diazepam
2nd line=antiepileptic drug IV eg phenytoin (will need cardiac monitoring) or sodium valproate
What is sudden onset headache with third cranial nerve palsy or painful third nerve palsy until proven otherwise?
Subarachnoid haemorrhage
Potential causes of sudden severe headaches?
SAH, cerebral venous sinus thrombosis, dissection-carotid/vertebral, infection-bacterial meningitis/encephalitis/cerebral abscess, acute haemorrhage/acute infarcts, pituitary apoplexy
What are SAHs usually caused by?
Rupture of saccular aneurysm
Signs and symptoms of SAH?
Acute severe localised headache (“hit by a hammer”)
Meningism (nausea, vomiting, stiff neck, photophobia)
Double vision
Ptsosis
Sometimes-sezures, low GCS, sudden death
Investigations after suspected SAH?
CT ASAP-sensitivity decreases with time
CTA or MRA
LP 12 hours after event
CSF xanthochromia if presenting late
How does GBS present?
Can be demyelinating or axonal, acute/subacute, immune mediated, multifocal polyradiculoneuritis
Numbness starts distally, progressive ascending weakness, bifacial weakness and other cranial neuropathies, flaccid tetra or paraperesis, areflexia
Potential different presentations: paraparetic, pharyngeal-cervical-brachial weakness, bifacial weakness with paraesthesia, Miller-Fisher syndrome (less severe form of GBS)
What are potential dangers of GBS?
Severe weakness, aspiration, resp failure, autonomic instability (severe sudden hypotension and cardiac arrhythmias)
Main management principles of GBS?
Monitor FVC and ECG
Always admit. Let ITU know early if VC less than 1L
DVT prophylaxis, BP, monitor swallow
How to treat GBS?
IV Ig or plasma exchange
When is a spinal cord emergency suspected?
What must be ruled out and how?
Acute/subacute onset bladder-bowel weakness saddle anaesthesia leg weakness constant sensory deficit significant pain
Rule out cord compression via MRI
What will a lesion of the R dorsal column at L1 result in?
Common causes?
Absences of light touch, proprioception and vibration in the right leg
Common causes= MS, penetrating injuries, tumour compression
What will a lesion of the R fasciculus cuneatus at C3 result in?
Common causes?
No light touch, vibration or proprioception in R arm and R trunk
Common causes= MS, penetrating injuries, tumour compression
What will a lesion of the R lateral corticospinal tract at L1 result in?
Common causes?
UMN signs in the R leg (weakness, hyperreflexia, hypertonia)
Common causes= penetrating injuries, lateral compression from tumours, MS
What will a lesion of the R lateral spinothalamic tract at L1 result in?
Common causes?
Absence of pain and temperature sensation in the left leg
Common causes= penetrating injuries, MS, compression from tumours
What will a lesion of the anterior gray and white commissures at C5-C6 result in?
Common causes?
Central cord syndrome!
Absence of pain and temperature sensation in c5 and c6 dermatomes in both upper extremities
Common causes= post traumatic contusion, syringomyelia, intrinsic spinal cord tumours
What will a complete transection of the R half of the spinal cord at L1 result in?
Common causes?
Brown-Sequard syndrome!
Absence of light touch, proprioception, vibration in R leg. UMN signs in R leg. Absence of pain and temperature sensation in L leg
Common causes=penetrating injuries, tumour compression, MS
What will complete transection of the spinal cord at L1 result in?
Common causes?
Both legs will have absence of light touch, vibration and proprioception. UMN signs in both legs/paraplegia. No pain or temp in either leg.
Common causes=trauma, tumours, transverse myelitis, MS
What will complete transection of the dorsal columns in the cervical region result in?
Common causes?
No light touch, vibration or proprioception from neck down
Common causes= trauma, posterior tumour compression, MS, vitamin B12 deficiency
What will complete transection of the lateral spinothalamic tracts with DC sparing in the cervical region result in?
Common causes?
Anterior cord syndrome!
UMN signs bilaterally below the lesion (damage to lateral corticospinal), LMN signs bilaterally at the level of the lesion (damage to LMN in ventral horns), no pain nor temp bilaterally below the lesion level
Common causes=anterior spinal artery occlusion, MS, occlusion of artery of Adamkiewicz during AAA repair
Presentation of cauda equina?
Common causes?
SPIN= saddle anaesthesia, pain/paralysis, incontinence bladder/bowel, numbness Causes= compressive (discs and tumours), non compressive- inflammatory/infiltrative/granulomatous, vascular (spinal dural fistula)
What are the different types of focal seizures?
Simple partial seizures (aura), complex partial seizures (loss of consciousness), secondary generalised tonic clonic seizures
What are the different types of generalised seizures?
Generalised tonic clonic seizures, myoclonic jerks, absences (a/w 3 second spike and wave on EEG)
Causes of syncope?
Reflex-vasovagal, situational, carotid sinus hypersensitivity
Cardiogenic- conditions that predispose to transiet tachyarrythmias, bradyarrhythmias, cardiac ischaemia, structural heart disease
Orthostatic hypotension- drugs, autonomic failure
What types of heart block have a high risk of progression to asystole?
Complete/3rd degree heart block
Mobitz type II 2nd degree heart block
Incomplete trifascicular block-RBBB, LAD, 1st degree heart block
TLOC during exercise is what type of TLOC until proven otherwise?
Cardiogenic
What are PNES?
Psychogenic non-epileptic seizure
Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges
Physical manifestation of psychological distress
A/w comorbid psychopathology and with childhood sexual abuse
Common features of a generalised tonic clonic seizure?
No trigger, may have aura, stiffening/jerking of limbs/vocalization or grunting/cyanosis/eyes open, 1-2 mins, post-ictal confusion for about 20 mins, lateral tongue bite, urinary incontinence, injury
NB/tramadol use lowers seizure threshold, and ask about alcohol/recreational drug use
Characteristics of syncope?
Triggers, typical fainting prodrome, pallor, may have jerks if in upright position, brief. No post-ictal period, rapid recovery. Look for hypotensive medications
Characteristics of PNES?
May be situational, eyes often closed, often wax and wane, may be emotional. Often very prolonged. Post ictal is variable but almost always tired/washed out
Look for antidepressants or psychotic medications. SH very important
Investigations for TLOC?
12 lead ECG for all TLOC
Neuroimaging- CT not indicated in syncope but in epilepsy (MRI is better)
EEG in very frequent seizures
Recordings of the event
Myotome, dermatome and reflex associated with c5/c6 root?
Elbow flexion, thumb, biceps reflex
Myotome, dermatome and reflex associated with c7 root?
Elbow extension, middle finger, triceps reflex
Myotome and dermatome a/w c8/t1 root?
Hand myotome and medial hand/forearm dermatome
Myotome, dermatome and reflex a/w L5 root?
Dorsiflexion
Dermatome=big toe, dorsum of foot
No reflexes
Myotome, dermatome and reflex a/w S1 root?
Plantarflexion
Little toe, sole and heel
Ankle jerk
Describe the normal volumes of the ventricular system?
CSF produced at 500ml/24 hour
Total CSF volume=120ml
Capacity of ventricular system=20ml
Normal pressure 5-15cm H2O
Symptoms and signs of hydrocephalus?
Symptoms: headache, vomiting, visual disturbance, gait unsteadiness
Signs: drowsiness, papilloedema, limitationof upward gaze, reduced visual acuity
Shapes of extradural haematoma and subdural haematoma on CT?
Extradural= lemon shaped Subdural= quarter moon
What are the characteristics of a migraine?
Moderate to severe
Unilateral and throbbing lasting 4-72 hours
Migraine with or without aura or silent migraine (aura and no headache)
Aura can last 5 minutes to an hour
May have prodromal stage (mood, energy levels, appetite, behaviour changes)
Often nausea, vomiting, photo/phonophobia
What could be in the aura phase of a migraine?
Visual problems-blind spots, flashing lights, zig-zag patterns
Numbness or tingling
Feeling dizzy or off balance
Dysphasia
Common triggers for migraines?
Menorrhoea, stress, tiredness, certain foods or drinks, exercise
How to treat a migraine?
Paracetamol/aspirin/ibuprofen can help reduce symptoms but beware medication overuse headache
Triptans (cause blood vessels around brain to constrict)
Anti-emetics
Transcranial magnetic stimulatoin
How to prevent migraines?
Topiramate (antiepileptic) Propranolol Amitriptyline Botulinum toxin type A for chronic migraine (headaches on over 15 days a month, 8 of which must be migraine) Acupuncture
What are the characteristics of a tension headache?
Bilateral ache
May feel neck muscles tighten and feeling of pressure behind eyes
Usually 30 mins-few hours but can last several days
Common causes of tension headaches?
Stress and anxiety, squinting, poor posture, tiredness, dehydration, missing meals, lack of exercise, bright sunlight, noise, certain smells
How to manage tension type headaches?
Simple analgesia
Relaxation techniques
Trigger avoidance
What are the characteristics of a cluster headache?
Excruciating, unilateral, often around the eye
More common in men, tend to start in 30s or 40s
Sharp, burning or piercing sensation
Associated symptoms: red or watering eye, ptosis and swelling of 1 eyelid, miosis in 1 eye, sweaty face, blocked or runny nostril
Lasts 15 mins to 3 hours, typically occur between 1-8 times a day
Often at same time of day
How to manage cluster headaches?
Specialist treatment: sumatriptan injections or nasal spray, o2 therapy, zolmitriptan nasal spray
Newer= transcutaneous vagus nerve stimulation.
Chronic=stimulation device implantation.
How to prevent cluster headaches?
Avoid triggers eg don’t drink alcohol during a cluster bout, avoid strong smelling chemicals, avoid exercise
Verapamil as soon as headache begins and continue until bout is stopped
If verapamil doesn’t work, consider corticosteroids, lithium and local anaesthetic injections into back of head
What are the characteristics of temporal arteritis?
Frequent, severe headaches
Pain and tenderness over temples
Jaw pain while eating or talking
Vision problems eg diplopia or loss of vision in 1 or both eyes
Highly associated with developing polymyalgia rheumatica
How to diagnose temporal arteritis?
Ultrasound scan of temples
Examination of temples- tender temporal arteries
Biopsy of temporal arteries (giant cell infiltration)
How to treat temporal arteritis?
Prednisolone
Initial high dose for a few weeks, then lower steroid dose for longer term
Potential others: low dose aspirin, PPIs, bisphosphonate therapy, immunosuppressants
Causes of cerebellar disorder?
Vascular (Stroke or TIA)
Space-occupying (hydrocephalus or posterior fossa tumours/abscesses)
Nutritional (Wernicke’s encephalopathy, vit E deficiency, gluten sensitivity)
Infections (meningo-encephalitis, HIV, toxoplasmosis, Creutzfeldt-jakob disease)
Toxins (alcohol, mercury, CO poisoning)
Drugs and drug OD
Trauma
MS
Genetic
Metabolic and endocrine (eg inherited metabolic disorders)
Congenital (eg cerebral palsy)
Idiopathic
Describe presentation of cerebellar disorder?
ATAXIA (different depending where in cerebellum) eg truncal, limb (lesions of cerebellar hemisphere cause ipsilateral signs), Riddoch’s sign, acute-onset, subacute, episodic, chronic progressive
DYSARTHRIA -spluttering stoccato speech
Larger writing
TREMOR- unilat, bilat or truncal
Nausea and vomiting
Cerebellar cognitive affective syndrome
DYSDIADOCHOKINESIS
NYSTAGMUS
May have mild hypotonia and hyporeflexia
Features of simple partial seizures?
Auras/Focal seizures without impaired consciousness
Most commonly from temporal lobes, sometimes frontal lobes, rarely other lobes
Focal motor signs, autonomic signs (flushing, sweating, vomiting), sensory signs (flashing lights, unpleasant odours, tastes, vertigo, pain, paraesthesia), psychic symptoms (deja vu, depersonalisation, fear)
Features of complex partial seizures?
Focal seizure with impaired consciousness
Automatic behaviours eg plucking at clothes, fiddling, lip smacking, chewing, grimacing
Post-ictal confusion and amnesia
Features of tonic-clonic seizure?
/Grand mal
Tonic stage= lose consciousness, body goes stiff and may fall to floor
Clonic stage= limbs jerk about, may have incontinence, may have lateral tongue bite
Post ictal drowsiness, confusion, headache, myalgia, incontinence
Features of an absence seizure?
/Petit mal
Lose awareness of surroundings, mainly affect children
stare blankly, look like daydreaming, flutter eyes, may make slight jerking movements of body and limbs.
Last up to 15 seconds and amnesia afterwards
Features of a myoclonic seizure?
Some or all of body suddenly twitches and jerks
Often happen soon after waking up
Last a few mins and might lose consciousness
Features of an atonic seizure?
All muscles relax so may fall to the ground, sudden loss of tone
Quick recovery
Features of a tonic seizure?
All muscles become rigid, maybe causing a fall
Quick recovery
Which anti-epileptic to prescribe for focal seizures?
Lamotrigine, Carbamazapine are first line
Which AED for tonic clonic seizures?
Sodium valproate or lamotrigine if not suitable
Which AED for absence seizures?
Ethosuximide or sodium valproate
Lamotrigine if above are unsuitable
Which AED for myoclonic seizures?
Sodium valproate
Topiramate if unsuitable
Features of narcolepsy?
Lack of hypocretin/orexin in brain (regulates wakefulness)
Excessive daytime sleepiness, sleep attacks, cataplexy, sleep paralysis, excessive dreaming and waking in the night
How to manage narcolepsy?
No cure
Frequent, brief, evenly spaced naps throughout the day
Strict bedtime routine
Stimulant medication eg modafinil, dexamphetamine, methylphenidate
Consider antidepressants
How to diagnose narcolepsy?
Rule out sleep apnoea, epilepsy, depression, hypothyroid and a previous head injury
See if secondary narcolepsy-head injury, brain tumour, MS, encephalitis
Sleep analysis- Epworth sleepiness scale, polysomnography, measure hypocretin levels
What is cataplexy?
Sudden temporary muscle weakness or loss of muscular control.
Commonly experienced by those with narcolepsy
Typical symptoms= jaw dropping, head slumping, leg collapsing, slurred speech, double vision
Usually triggered by strong emotions
How to manage cataplexy?
Sodium oxybate
Antidepressants eg fluoxetine, venlafaxine, imipramine
What is shingles/what causes it?
Viral infection by varicella-zoster virus
After chickenpox virus lies inactive in nerve tissue near nervous system, when it reactivates=shingles
Describe the presentation of shingles?
First signs=tingling or pain in an area of skin, headache or feeling unwell
Unilateral itchy rash after a few days- red blotches, then itchy blisters, then scabbed over, painful skin after the rash has gone
Can take up to 4 weeks for rash to heal
Potential complications of shingles?
Postherpetic neuralgia
Vision loss (ophthlmic shingles)
Neurological problems eg encephalitis, facial paralysis, hearing/balance problems
Skin infections of blisters
Management of shingles?
Avoid pregnant women who haven’t had chickenpox, people with weakened immune system, babies less than 1 month
Shingles vaccination for people in their 70s
Paracetamol, keep rash clean, wear loose-fitting clothing, cool compress
What is the pathaphysiology of Wernicke-Korsakoff syndrome?
Drinking alcohol prevents body from getting enough thiamine/vit B1- this is vital for neurones to work
2 stages
stage 1=intense inflammation=wernicke’s encephalopathy
stage 2=if encephalopathy not treated quickly, may developl korsakoff’s syndrome=similar to dementia
What are the symptoms of wernicke’s encephalopathy?
Disorientation, confusion and mild memory loss (most common sxs)
Difficulty controlling eye movements-nystagmus and conjugate gaze palsies
Poor balance, wide based gait
Undernourished
Triad= acute confusion, ataxia, ophthalmoplegia
How to manage suspected wernicke’s encephalopathy?
May need MRI to confirm
Immediately stop drinking alcohol
High dose IV thiamine hydrochloride
Causes of wernicke’s encephalopathy?
90% cases=alcohol abuse
Also could be:
Starvation, postbariatric surgery, GI malignancy, chronic dialysis
What are the symptoms of Korsakoff’s syndrome/Wernicke-Korsakoff syndrome?
Confabulation and memory loss (global amnesia)
What is the pathaphysiology of Huntington’s disease?
CAG triplet expansion repeat in the huntingtin gene
Number of repeats determines phenotype eg over 39=100% penetrance
Autosomal dominant, shows anticipation
Presentation of Huntington’s disease?
Neuropsychiatric=progressive personality change, behavioural abnormalities, depression, cognitive impairment, psychosis
Motor= chorea, parkinsonism, dystonia, slowing of saccades
Weight loss
What is the treatment of Huntington’s disease?
No disease-modifying treatment
Supportive
Atypical antipsychotics-dual action on chorea and psychosis
Symptom support-chorea, depression, psychosis
Death usually within 15-20 years of diagnosis
How can you manage chorea?
Atypical antipsychotics, tetrabenazine, amantadine
What is the pathaphysiology of Parkinson’s disease?
neurodegenerative a/w Lewy bodies
loss of dopaminergic neurons in the substantia nigra pars compacta
imbalance of dopamine and ACh in striatum
What are the symptoms of parkinson’s disease?
Bradykinesia/hypokinesia, resting tremor, rigidity, postural instability
Loss of sense of smell, constipation, urinary frequency/urgency, REM sleep disorder, visual hallucinations, sialorrhoea, depression/memory impairment
What could you see on examination of a person with Parkinson’s disease?
Hypomimia, quiet speech Cranial nerves are normal Lead-pipe rigidity Cog-wheeling Resting tremor 4Hz (3-5) Brady/hypokinesia Stooped posture Shuffling gait, unilateral reduced arm swing, freezing of gait Postural instability Micrographia
What are the treatments for parkinson’s disease?
Speech therapy and physio. Deep brain stimulation
Levodopa, dopamine agonists, MAO B inhibitors, anticholinergic agents, amantadine, COMT inhibitors
Pros and cons of levodopa?
pros= most effective drug for bradykinesia/akinesia, some improvement in tremor/rigidity. Can be combined with peripheral decarboxylase inhibitor to prevent postural hypotension eg levodopa+carbidopa=sinemet, levodopa+benserazide=madopar
Cons=rarely improves postural instability, nausea at first, GI absorption varies with different meals, motor fluctuations (get worse with longer duration)-dyskinesia/wearing-off/dystonic posturing
Examples of dopamine agonists?
Pramipexole, ropinirole, bromocriptine, cabergoline, rotigotine, apomorphine
Issues with dopamine agonists?
nausea, somnolence, a/w mood disorders and impulse control disorders, withdrawal syndrome. Can sometimes cause confusion and hallucinations.
What leads to vascular dementia?
Any ischaemia/hypoperfusion of brain tissue eg TIA and stroke
How to diagnose vascular dementia?
Clinical assessment and history
CT or MRI
What are the symptoms of Alzheimer’s disease?
Early stages=memory lapses
Middle stages=increasing confusion and disorientation, obsessive/repetitive/impulsive behaviour, delusions, aphasia, disturbed sleep, mood changes, hallucinations
Later stages=hallucinations and delusions can get worse, dysphagia, weight loss, incontinence, gradual loss of speech, significant memory problems (short and long term)
What is the pathaphysiology of Alzheimer’s disease?
Amyloid deposits forming plaques in neural tissue
Tau deposits-neurofibrillary tangles
Decreased ACh
Atrophy of brain
How to treat Alzheimer’s disease?
No cure
Acetylcholinesterase inhibitors eg donepezil, galantamine and rivastigmine for early-mid stage disease
Memantine (blocks glutamate receptor) for mod-severe
BPSDs-coping strategies, risperidone/haloperidol if absolutely necessary
Social support
What are BPSDs?
Behavioural and psychological symptoms of dementia:
eg increased agitation, anxiety, wandering, aggression, delusions and hallucinations
What is the pathaphysiology of normal pressure hydrocephalus?
Primary NPH=idiopathic (most)
Secondary NPH= previous IVH/SAH/scarring from meningitis
Abnormal build up of CSF leading to ventricular enlargement with a normal LP opening pressure
What are the signs and symptoms of NPH?
Magnetic gait-bilateral
Cognitive disturbance-psychomotor behaviour deficits and bradyphrenia (dementia like symptoms)
Urinary urgency progressing to incontinence
How to diagnose NPH?
Firm diagnosis can’t be made-categories as either probably, possible or unlikely NPH
MRI head: lat and third ventricles out of proportion to sulcal enlargement
CSF flow studies
How to treat NPH?
Neurosurgery for consideration of VP shunt
What are the 3 types of hydrocephalus?
Congenital, acquired, normal pressure
Also communicating and non-communicating
What can cause congenital hydrocephalus?
What are the potential complications?
Spina bifida, maternal infection eg mumps or rubella
Long-term complications:
learning disabilities, speech and memory problems, short attention span, vision problems eg squint or vision loss, epilepsy, coordination issue
What can cause acquired hydrocephalus?
Brain or spinal cord tumours, infections of CNS eg bacterial meningitis, injury or stroke
Signs and symptoms of acquired hydrocephalus?
Headaches (may be worse in the morning). Neck pain, nausea, vomiting, sleepiness, confusion, blurred vision or diplopia, gait disorders, incontinence
Signs and symptoms of hydrocephalus in infants?
Rapid increase in head size, unusually large head, bulge on fontanel, vomiting, feeding issues, sleepiness, irritability, eyes fixed downwards (“sun setting”), seizures
How to treat hydrocephalus?
Shunt or endoscopic third ventriculostomy (ETV)
Rehab therapies ad educational interventions
What is the commonest form of brain tumour?
Brain metastases, commonly from lung/melanoma/breast
Potential presentations of brain tumours?
Raised ICP-vomiting, diplopia
Headache-dull, constant or throbbing, progressive, may be worse at night and waking the patient
Seizures
Focal deficits-weakness, sensory loss, aphasia
What are the different types of primary brain tumour?
Meningioma (1/3 of primary)
Gliomas (around 1/3 of primary); astrocytoma, oligodendroglioma, ependymoma, schwannoma, craniopharyngioma
Describe a meningioma
Attached to dura (10% arise from spinal cord)
Slow growing, often asymptomatic and incidental findingss
More common in older female patients
Describe a glioma
Fast growing generally and normally younger patients
Describe the brain tumour grading/classification (WHO)
Grade I= lowest grade tumours eg pilocytic astrocytoma
Grade II= lower grade malignancies eg fibrillary astrocytoma
Grade III= higher grade malignancies eg anaplastic astrocytoma
Grade IV= highest-grade malignancies eg glioblastoma multiforme
Describe the pathaphysiology of multiple sclerosis
Autoimmune inflammatory disorder of CNS characterised by widespread demyelination throughout CNS as well as diffuse neuronal loss (degeneration of oligodendrocytes)
Describe the epidemiology of MS
RFs: onset generally in 20s, female (2:1), smoking, EBV exposure, low vitamin D, childhood obesity, genetics-HLA-DRB1
What are the different forms of MS?
Relapse-onset (95%)
Progressive-onset (5%)
What are the most characteristic syndromes seen at initial presentation and relapse in MS?
Optic neuritis, transverse myelitis, sensory disturbance, UMN weakness, cerebellar syndrome, brainstem syndromes eg internuclear ophthalmoplegia
What is Lhermitte’s sign?
Paroxysmal shock-like sensations down back and limbs on neck flexion in MS
What is Uhtoff’s phenomenon?
Paroxysmal worsening of symptoms on heat exposure in MS
What is the MacDonal 2010 criteria?
For a diagnosis of MS: dissemination in space (relapse and radiological) and dissemination in time (clinical and radiological)
What can be seen on LP in MS?
Oligoclonal bands
How would you treat a relapse of MS?
Steroids
What disease modifying therapies are available for MS?
(No proven benefit in progressive MS)
Interferon beta, glatirameracetate, daclizumab, natalizumab, alemtuzumab, fingolimod
What management options have proven benefit in progressive MS?
Ocrelizumab
Haematopoietic stem cell transplantation
What symptomatic treatment can you use in MS?
Nociceptive pain-NSAIDs, TENS, physio Neuropathic pain-gabapentin, amitryptilline, TENS Trigeminal neuralgia-Carbamazapine Bladder dysfunction-self catheterisation Spasticity-baclofen
What are the different types of MND?
Amyotrophic lateral sclerosis, Progressive muscular atrophy, primary lateral sclerosis, progressive bulbar palsy, flail arm syndrome
How does ALS manifest?
Begins with distal, asymmetric limb weakness which progresses proximally
Limb muscles: UMN and LMN signs
Bulbar muscles; dysarthria, dysphagia, pseduobulbar effect (sudden inappropriate laughing or crying, uncontrollable)
Axial muscles: head drop, postural instability
Respiratory muscles: initially dyspnoea on exertion and nocturnal hypoventilation, later=neuromuscular resp failure
Cognitive=a/w frontotemporal dementia
How to diagnose MND?
Exclusion of differentials-bloods, LP, EMG, NCS (reduction in number of motor axons), MRI brain and spinal cord
What treatment options are there for MND?
Supportive care eg baclofen for spasticity, SLT, alternative feeding routes, NIV, tracheostomy, muscarinic antagonists eg hyoscine hydrobromide for sialorrhoea
Riluzole= disease-modifying drug, extends survival by a few months and extends tracheostomy-free survival
What are the symptoms of cerebral palsy and when do you notice them?
Start to notice symptoms during first 2-3 years of life
Problems with movement, coordination and developmemt eg developmental milestone delays, hypotonia, weakness, clumsy movements, spasms, tremors, walking on tiptoes
Potential other symptoms: feeding/drooling/swallow issues, constipation, speaking issues, epilepsy, GORD, scoliosis, dislocating hips, urinary incontinence, hearing loss, learning disability, squint/reduced vision
What are the 4 main types of cerebral palsy?
Spastic cerebral palsy-rigidity
Dyskinetic cerebral palsy -switch between rigidity and floppiness
Ataxic cerebral palsy- balance and coordination issues
Mixed cerebral palsy
Causes of cerebral palsy?
Prenatal issues: periventricular leukomalacia, maternal infection eg rubella and toxoplasmosis, stroke, injury to unborn baby’s head
Problems during or after birth: asphyxiation during difficult birth, meningitis, serious head injury, choking or nearly drowning, very hypoglycaemic, stroke
Risks: premature birth, low birthweight, part of multiple birth, mother taking cocaine/smoking/drinking
How to diagnose cerebral palsy?
MRI or cranial ultrasound
EEG if seizures
General lab tests
Identify where issues are eg vision, hearing, speech, intellect, development and movement
What is neurofibromatosis type 1?
Autosomal dominant genetic condition causing (usually benign) tumours to grow along nerves
What are the symptoms of neurofibromatosis type 1?
Often mild and no serious health problems
Skin: cafe au lait spots, freckles in unusual places eg armpits, tumours on or under skin=neurofibromas
Some children develop learning and behavioural problems-ADHD and ASD
Tumour on optic pathway (optic pathway glioma)-rarely symptomatic but may interfere with vision
Some develop hypertension due to renal artery stenosis
Physical development: scoliosis, bigger head, small size and lower weight
Migraines, rarely brain tumours
What is the treatment for NF1?
Regular monitoring. May include physio, psychological support and pain management
What are the main symptoms of neurofibromatosis type 2?
Tumours leading to hearing loss, tinnitus and balance problems
Cataracts
Skin tumours
Peripheral neuropathy
Brain: headaches, vomiting, seizures, visual disturbances
Spinal cord: back pain, muscle weakness, unpleasant sensations
What is mosaic NF2?
Milder form of NF2 where symptoms are milder and often restricted to certain area or side of body
What monitoring is required in NF2?
Annual MRI scans
Annual eye tests for cataracts
Annual hearing tests
What are the causes of meningitis?
Bacterial: Streptococcus pneumoniae, Neisseira meningitidis, Listeria monocytogenes (elderly and immunocompromised), Haemophilus influenzae (children), Gram negatives (elderly and immunosuppressed), TB (immunosuppressed), staphylcocci (neurosurgery patients)
Fungal: cryptococcus neoformans
Viral: HSV2, enterovirus
What is the presentation of bacterial meningitis?
Fever, headache, meningism (photophobia and neck stiffness), confusion/decreased GCS, sepsis developing over a few days
What could be seen on examination of someone with bacterial meningitis?
Septic, rash (non-blanching, petechial/purpuric)
Decreased GCS
Cranial neuropathis, papilloedema
Meningism: photophobia, neck stiffness (passive and active), Brudzinski sign and Kernig’s sign
What is Brudzinksi’s sign?
Neck flexion leading to hip flexion
What is Kernig’s sign?
Hip flexion prevents knee extension
How to investigate for bacterial menigitis?
Bloods-culture, FBC, U+E, coagulation: neutrophilia and increased CRP
LP: increased WCC (neutrophilia), increased protein, decreased glucose
CT head-prior to LP if decreased GCS/raised ICP/focal neurological deficit/seizures
What antibiotics for bacterial meningitis?
In GP: IM or IV benzylpenicillin asap
Secondary care: initially empiric then narrow once cultured. Ceftriaxone. Add ampicillin for elderly/immunocompromised.
Overall management of bacterial menigitis?
IV antibiotics Dexamethasone in pneumococcal disease Iv fluids Treat close contacts with oral ciprofloxacin Notify PHE
What is the pathaphysiology of encephalitis?
Inflammation of the brain. Usually caused by virus (most commonly=herpes simplex virus). Potential other viruses=mumps, measles, flu, varicella zoster virus.
What are the symptoms of encephalitis?
Fever, headache, muscle aches, tired, nausea and vomiting
Meningism, coma, seizures
How to diagnose encephalitis?
CT or MRI to rule out other causes and rule out signs of raised ICP
LP, bloods.
May have EEG
How to manage encephalitis?
Antiviral-aciclovir without hesitation
Antibiotics if suspecting meningitis
Supportive: fluids, antipyretic, oxygen etc
What is horner’s syndrome?
Disruption of sympathetic nerves supplying the eye
Triad of partial ptosis, miosis (leading to anisocoria/difference in size of pupils) and anhidrosis
What is the presentation of horner’s syndrome?
Ptosis, anhidrosis, facial flushing if preganglionic lesion, orbital pain/headache is postganglionic lesion
Name some potential causes of Horner’s syndrome
Central (first order) nerve lesions: stroke, MS, pituitary tumour, basal meningitis, neck trauma, syringomyelia
Preganglionic (second order) nerve lesions: apical lung tumour eg Pancoast, lymphadenopathy, lower brachial plexus trauma, aortic aneurysms, trauma to chest, neuroblastoma
Postganglionic (third order) nerve lesions: cluster headaches or migraine, herpes zoster, internal carotid dissection, temporal arteritis
How can you test for Horner’s?
Cocaine eye drops- dilation of pupil normally, but no response in Horner’s syndrome
Apraclonidine-little effect on normal pupil but causes dilation of Horner’s pupil
How can you classify strabismus?
Congenital or acquired Right, left or alternating Permanent or intermittent Manifest or latent Concomitant (non-paralytic-size of deviation does not vary with direction of gaze) or incomitant (paralytic-direction of gaze does affect size) Primary secondary or consecutive Infantile Situational
How to examine for strabismus?
Hirschberg’s test (pen torch should be central bilaterally, if lies on inner margin of the pupil=exotropia, if on outer margin=esotropia)
Cover/uncover test
Alternate cover test
What normally causes paralytic squint?
Damage to extraocular muscles of their nerves- CN III, IV, VI
Isolated nerve palsy or multiple nerves
Myopathies- tend to be bilateral
Describe presentation of third nerve cranial palsy?
Common causes?
External ophthalmoplegia with partial or complete mobility problems (various degress of squint), may be internal ophthalmoplegia (partial or incomplete impairment of pupillary reactions)
Ptosis
CC: aneurysm, tumour, trauma, pituitary apoplexy, herpes zoster, leukaemia. Ischaemic microvascular disease=pupil sparing
Describe presentation of fourth nerve palsy?
Common causes?
Binocular vertical diplopia, difficulty reading, sense that things are tilted
CC: trauma, vasculopathy, demyelinating disease
Describe presentation of sixth cranial nerve palsy?
Common causes?
Horizontal diplopia which is worse for distance than near vision and most pronounces on lateral gaze on affected side
CC: vasculopathy and trauma, idiopathic
What might be the cause of multiple nerve palsies causing strabismus?
Arteriovenous fistula, cavernous sinus tumours, pituitary apoplexy, herpes zoster, cavernous sinus thrombosis
Differences between UMN and LMN lesions of facial nerve?
UMN= only affect lower face due to contralateral innervation
LMN=ipsilateral weakness of entire face
What is the potential presentation of Bell’s Palsy?
Sudden weakness of one side of the face. Not forehead sparing. May have drooping of the mouth, drooling, inability to close eye, excessive tearing in one eye. May have impaired or altered sense of taste and sensitivity to loud noise
How to manage Bell’s Palsy?
Try to see within 72 hours of onset. Steroids (prednisolone) and antiviral medication (aciclovir)
What are the clinical features of facial nerve lesions?
Weakness of muscles of facial expression, hyperacusis, impaired corneal reflex (afferent CN V efferent CN VII), dry eyes, dry mouth, loss of taste in anterior 2/3 of tongue
What are the symptoms of trigeminal neuralgia?
Episodes of brief, sharp, stabbing pain in trigeminal (usually V2 or V3) nerve distribution triggered by light touch, cold air or facial movements
Episodes last for seconds and followed by refractory period during which further attacks do not occur
Causes of trigeminal neurlagia?
Classical=idiopathic
Peripheral causes= herpes zoster, trauma, cavernous sinus lesions
CNS causes=demyelination, infarction
How to manage trigeminal neuralgia?
Treat underlying causes eg if due to grinding teeth, wear a mouth guard
First line=carbamazapine (not nice), nicer=amitriptyline
What is bovine papular stomatitis?
A virus that affects cattle, can be transmitted to humans
What is bulbar palsy?
Result of diseases affecting lower cranial nerves VII-XII. Speech deficit due to paralysis or weakness of muscles of articulation
Causes of bulbar palsy?
Broad classification= muscle disorders, diseases of motor nuclei in medulla and lower pons, intramedullary nerves of spinal cord diseases, diseases of peripheral nerves supplying the muscles
Examples: diphtheria, poliomyelitis, MND, syringobulbia, brainstem tumours, GBS
Presentation of bulbar palsy?
Tremulous lips, weak and wasted tongue with fasciculations, drooling, absent palatal movements, dsyphonia (rasping tone due to vocal cord paralysis, nasal tone if bilat palatal paralysis), articulation-difficulty pronouncing r sounds and progressively can’t do consonants
What is pseudobulbar palsy?
Results from disease of corticobulbar tracts.
Presentation of pseudobulbar palsy?
Paralysed tongue, palatal movements absent, persistent dribbling, facial muscles may also be paralysed, exaggerated reflexes, nasal regurg, dysphonia, dysphagic, emotional lability may be present
Causes of pseudobulbar palsy?
Cerebrovascular events, demyelinating disorders, MND, high brainstem tumours, head injury, neurosyphilis
What is sciatica?
Sciatic nerve (L4-S3) irritated or compressed Pain radiating along path of sciatic nerve, branching from lower back down through hips, buttocks and down leg. Commonly due to herniated disk or bone spur or spinal stenosis
Symptoms of sciatica?
Pain radiating from lumbar spine to buttock and down back of leg, to a level below the knee, sometimes felt in foot and great toe.
Some may experience numbness, tingling or muscle weakness. Prolonged sitting can aggravate. Normally unilateral.
How to manage sciatica?
Exercises and stretches. Physiotherapy.
Consider analgesia- NSAIDs or may need specific treatment for neuropathic pain eg gabapentin or amitriptyline
Define radiculopathy?
Condition due to compressed nerve in the spine
What is sciatica?
Sciatic nerve (L4-S3) irritated or compressed Pain radiating along path of sciatic nerve, branching from lower back down through hips, buttocks and down leg. Commonly due to herniated disk or bone spur or spinal stenosis
Symptoms of sciatica?
Pain radiating from lumbar spine to buttock and down back of leg, to a level below the knee, sometimes felt in foot and great toe.
Some may experience numbness, tingling or muscle weakness. Prolonged sitting can aggravate. Normally unilateral.
How to manage sciatica?
Exercises and stretches. Physiotherapy.
Consider analgesia- NSAIDs or may need specific treatment for neuropathic pain eg gabapentin or amitriptyline
Define radiculopathy?
Condition due to compressed nerve in the spine
What causes spinal stenosis?
Natural ageing process normally-degenerative changes leading to partial constriction
What do patients with spinal stenosis normally complain of?
Back and leg pain on walking, numbness or weakness, both legs or just one.
Classically can walk 50-500m and then have to stop as pain and numbness gets worse.
Improvement on sitting down or leaning forward
Normally no pain in the leg at rest
How to manage spinal stenosis?
First: simple analgesia, improve mobility/strength/fitness, weight loss if applicable, walking as best as possible, static bike cycling, may need neuropathic analgesia
Second: may need spinal injections, nerve blocks, consider surgery
What is anterior cord syndrome?
Incomplete cord syndrome predominantly affecting anterior 2/3 of spinal cord
Motor paralysis below level of lesion and loss of pain and temperature at and below level of lesion. Fine touch/vibration/proprioception spared
Normally due to ischaemia of that portion due to anterior spinal artery reduced blood flow- commonly aortic surgery
What is brain herniation?
Life-threatening condition with shift of brain tissue into adjacent space due to mass effect
Different patterns: subfalcine, transalar, transtentorial (uncal and central, ascending), tonsillar, extracranial, paradoxical
What could cause brain herniation?
Any intracranial mass: intracranial haemorrhage (extradural, subdural, intracerebral), cerebral swelling (infarction, periabscess oedema), tumours, cerebral abscess
If signs of raised ICP, should you do a LP?
NO- can lead to herniation!! Acute pressure gradient resulting in downwards displacement of cerebrum and brainstem
Difference between coma and stupor?
Coma= unrepsonsive, unrousable state
Stupor= unresponsive, rousable state
Potential causes of coma
Post-ictal
Anoxic
Metabolic-hypoglycaemia, hyponatraemia, acidaemia, uraemia, liver failure, myxoedema, Wernicke encephalopathy
Toxic-opiates, benzos, tricyclics, alcohol, neuroleptics
Coma with focal signs: vascular event
Coma with signs of meningism: SAH, meningitis, encephalitis
How to initially assess coma?
Resuscitation: Airway and C spine Breathing Circulation Diabetes ( 50ml 50% dextrose, consider thiamine if suspicious of Wernicke's) Drugs (consider naloxone) Epilepsy (if ongoing, lorazepam) Fever (meningitis, encephalitis?) GCS Herniation (evidence of coning-pupil, check tone and reflexes in all 4 limbs) Investigate
What will opiate misuse pupils look like?
Pinpoint, equal ,unreactive
What will a pontine lesion pupils look like?
Pinpoint, equal
What will metabolic encephalopathy pupils look like?
Small and reactive, equal
Symptoms of a brain abscess?
May develop quickly or slowly Headache (severe, localised, can't be relieved by pain killers) Changes in mental state eg confusio Nerve function- weakness, slurred speceh or paralysis Fever Seizures Nausea and vomiting Stiff neck Visual changes
NEUROLOGICAL EMERGENCY
What causes of brain abscess?
Infection in the skull- half the cases; persistent otitis media, sinusitis or mastoiditis
Infection through bloodstream (1 in 4 cases), immunocompromised especially. Cyanotic heat disease, pulmonary AV fistula, dental abscess, lung infections, endocarditis, peritonitis, cystitis
Infection after a head injury- (1 in 10 cases)- skull fracture due to penetrating injury, gunshot/shrapnel wound
rarely a complication of neurosurgery
How to treat a brain abscess?
IV antibiotics or antifungal if several absecesses, small (<2cm), deep, menigitis coexisting, hydrocephalus
Surgery and then antibiotics after : simple aspiration (burr hole using CT scan) or craniotomy
Describe steroid myopathy?
Management?
Arms, legs and pelvis symmetrically affected most
Increasing intolerance to exercise as muscles weaken with use and pain increases
Mx: reduce or stop steroids. Increase muscle strength. If not possible to stop, switch fluorinated steroids eg dexamethasone to nonflourinated eg prenisone
What are the inflammatory myopathies?
Chronic (long-standing) muscle inflammation, muscle weakness and sometimes muscle pain
Polymyositis, dermatomyositis, inclusion body myositis, necrotising autoimmune myopathy
Describe polymyositis
Affects skeletal muscle, bilaterally. Onset normally between 30 and 60.
Variable presentation. Untreated may lead to issues with swallow, speaking, rising from seated, climbing stairs, lifting objects
Describe dermatomyositis
Skin rash (patchy, purple or red) preceding or accompanying progressive muscle weakness
Rash usually on eyelids or on muscles used to extend joints
Describe inclusion body myositis
Most common form of inflammatory myopathy in people over 50, more common in men
Slow progressive muscle weakness and wasting of proximal and distal muscles (typically thighs and forearms), bilat usually. Multi-protein aggregates
Falling and tripping usually first noticeable symptoms. Weakness in wrists and fingers. Difficulty swallowing in half of cases.
Describe necrotising autoimmune myopathy
Weakness in upper and lower body. Similar to polymyositis and dermatomyositis.
Occurs alone or after viral infections, a/w cancer, in connective tissue disorders or in statins
How to diagnose inflammatory myopathies?
Bloods-muscle enzymes and autoantibodies, physical exam, biopsy
How to manage chronic inflammatory myopathies?
Cannot be cured but symptomatic management- medication, physical therapy, exercise, heat therapy, orthotics and assistive devices, rest
High dose steroids. May consider immunosuppressants
Name 2 metabolic myopathies
Myopathies due to something lacking-rare
Carnitine deficiency, lactate dehydrogenase deficiency, phosphoglycerate kinase deficiency,
Describe myotonic dystrophy
Genetic condition causing progressive muscle weakness and wasting
Typically affects skeletal muscle and commonly electrical conduction system of heart, resp, swallow, bowel etc
Describe statin induced myopathy
Spectrum: myalgia, myositis, rhabdomyolysis, asx increase in concentration of creatine kinase
Commonly: fatigue, flu-like symptoms, nocturnal cramping
Describe muscular dystrophy
Inherited diseases with a lack of dystrophin- causes problems with walking, swallowing and muscle coordination
Name some of the better known muscular dystrophies
Duchenne, Becker, congenital, myotonic, limb-girdle, facioscapulohumeral (FSHD), emery-dreifuss, distal muscular
What are the symptoms of poliomyelitis?
Flu-like illness 3 to 21 days after infection
Polio virus can attack nerves in spine and base of brain, causing paralysis usually in legs
Potential long term problems of polio
Muscle weakness, atrophy, contractures, deformities
Describe the cervical dermatomes
c2= temple and forehead
c3=neck, posterior cheek
c4= shoulder, clavicle, upper scapula
c5=deltoid, anterior aspect of arm and base of thumb
c6=anterior arm, radial side of and to thumb and index finger
c7=lateral arm and forearm to index, long and ring fingers
c8=medial arm and forearm to fingers (long, ring, little)
Describe the thoracic dermatomes
t1=medial side of forearm to base of little finger
t2=medial side of upper arm to medial elbow
t3-t6=upper thorax
t5-t7=costal margin
t8-t12=abdomen and lumbar region
Describe the lumbar dermatoms
l1=back, trochanter and groin
l2=back, front of thigh to knee
l3=back, upper buttock, anterior thigh and knee, medial lower leg
l4=medial buttock, lateral thigh, medial leg, dorsum of foot, big toe
l5=buttock, posterior and lateral thigh , lateral leg, dorsum of foot, medial half of sole, first/second/third toes
describe the sacral dermatomes
s1=buttock, thigh and posterior leg
s2=buttock, thigh and posterior leg
s3=groin, medial thigh to knee
s4=perineum, genitals, lower sacrum
myotome c5 action?
shoulder abduction
what myotome for elbow flexion and wrist extension?
c6
c7 myotome action?
elbow extension
What myotome for finger flexion?
c8
what does t1 do?
finger abduction
myotome for hip flexion?
l2
myotome for knee extension?
l3
myotome l4 action?
ankle dorsiflexion
myotome l5 action?
great toe extension
what does s1 do?
ankle plantarflexion
What are potential causes of myopathies?
steroids, inflammatory, metabolic, myotonic, statin, muscular dystrophy, polio
Describe primary lateral sclerosis
Loss of cells in the motor cortex. UMN signs only
Describe progressive muscular atrophy
LMN only, distal before proximal muscles affected. Has the best prognosis for MND
Describe progressive bulbar palsy
CN ix-xii affected= palsy on tongue, muscles of chewing and facial muscles affected due to loss of function of brainstem nuclei. Carries worst prognosis
What are these repeats for?
GAA, CTG, CGG, CAG
GAA=Friedrich’s ataxia
CTG=myotonic dystrophy
CGG=fragile X syndrome
CAG=Hungtington’s
What are the features of Parkinson’s plus syndromes?
Bilateral, symmetrical symptoms, eye signs=progressive supranuclear palsy (impaired vertical gaze, nasal donald-duck voice secondary to pseduobulbar palsy, increaseing frequency of falls)
What is transient global amnesia? How to manage?
Transient loss of memory function, repeatedly ask the same question, no recall of events after the attack
Unknown aetiology
Mx= reassurance
Describe an essential tremor
Most common cause of titubation
Relieved by alcohol and sleep. Worse on movement and during stress
Can be fh (autosomal dominant)
Management of essential tremor
Propranolol first line
Primidone can be used
Potential causes of chorea
HD, SLE, pregnancy, thyrotoxicosis, wilson’s disease, ataxic telangiectasia, anti-phospholipid, oral contraceptive pill, l-dopa, antipsychotics
How to differentiate between essential tremor and pd?
DAT scan
What are the autonomic symptoms that can be experienced in PD?
orthostatic hypotension, constipation, N/V, urinary symptoms, seborrhoea, heat intolerance, sexual dysfunction, hypersalivation, sweating
Features indicative of idiopathic intracranial htn
BMI (obese), symptoms of raised ICP
What drug in brain herniation
Mannitol
Low GCS, slow breathing, pin point pupils?
Management?
Opiate OD
Naloxone (short half life)
Low GCS, slow breathing, normal pupils?
Management?
Benzo OD
Flumazenil (huge caution in epilepsy)
Pupils big and arrhythmia?
Tricyclic OD
No specific treatment
