My Neurology

• Faint
• Fit
• Funny turn (meabolic/traumatic/psychiatric cause)

• Patient's opinion: Feeling before/after and during
• Witness opinion: What happened before/after/during
• Risk factors for epilepsy
• Past history

• Commonly related to a trigger
• Prodromes always present
• Gradual onset (dizziness, loss of vision) but short duration and rapid recovery
• Convulsive jerks can occur
• Incontinence/tongue biting uncommon
• No confusion afterwards

• Triggers rare
• Prodromes common
• Sudden onset
• 1-3 minute duration
• Jerks frequent and prolonged
• Incontinence/tongue biting uncommon
• Confusion/amnesia afterward with slow recovery

• A sustained and synchronised cortical discharge, causing an excitation/inhibition imbalance
• Generalised tonic-clonic: potential amplitude/frequency steadily decrease causing tonic (rigid collapse) and clonic (twitching) stages
• Partial: Loss of awareness or cortical phenomena

• ECG: Always given after any blackout
• Blood glucose: Hypoglycaemia common cause of collapse
• MRI/CT: Rule out many mimicking or causative diseases
• EEG: Used for prognosis after seizure diagnosed

• Risk factors assessed uding EEG and CT/MRI
• Treatment not usually given unless risk of another seizure is above 60% (generally after 2 seizures)
• Localised seizures: Lamotrigine, carbamazepine
• Generalised seizures: Valproate

• Either:
• A seizure which carries on for 30 minutes or more
• A series of seizures with no regaining of consciousness in between them

• First aid
• Benzodiazepines: Relax muscles, but can only be used twice
• Phenytoin: Antiepileptic which stabilises voltage-gated sodium channels in inactive state = suppressed brain activity

• Epilepsy is the tendency to have recurrent, unprovoked seizures
• Localised onset: Begin in an area of abnormality with the rest of the brain normal
• Generalised onset: Usually genetic/congenital neurotransmitter imbalance

• 3rd most common cause of death
• Frequent cause of disability
• Consumes 5% of the NHS budget

Rapidly developing clinical signs of focal/global disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than a vascular one

• Ischaemic: 80% of cases - reduce blood flow from blockage/hypoperfusion
• Intra-cerebral haemorrhage: 15-20%, small vessels perpendicular to the MCAs rupture in hypertension
• Lacunar: Small perforating arteries (supply basal ganglia) rupture/stenose in hypertension

• Excitotoxicity: Loss of ATP causes reduction in K/NA pump action = potassium exits/sodium enters = H20 entry and swelling
• Glutamate: Released due to potassium exit = increased calcium = protease activation = apoptosis
• Inflammation: Causes infiltration/cell death

• Core: Main affected area, with unsalvageable necrotic tissue
• Penumbra: Halo of semi-ischaemic tissue, salveagable with emergency treatment
• Oligaemia: Very slightly ischaemic area

• Total anterior circulation stroke; damages one anterior hemisphere e.g. MCA occlusion
• Presents with:
• Contralateral hemiparesis
• Homonymous hemianopia
• Higher dysfunction (aphasia, memory loss, agnosia)

• PACS: Partial anterior circulation stroke; 2/3 of TACS clinical features
• LACS: Lacunar ACS, affects small area with features varying
• PCS: Posterior circulation stroke; affects CNs, stem or cerebellum

• DANISH:
• Disdiadochokinesis
• Ataxia
• Nystagmus
• Intention tremor
• Slurred speech
• Hypotonia

• Seizure
• Hypoglycaemia
• Infection
• Toxic-metabolic
• Neoplasia
• Syncope/CV disease

• Acute rise in BP (maintains CPP)
• Neuro exam
• ECG for AF, IE
• Bloods: Obs, coag, FBC, U+Es, lipids, glucose
• Imaging: CT/MRI for space occupying lesion

• After BP, BM and coagulation screen performed, transferred
• Thrombolysis given within 'window'; 4.5 hours
• Carotid endartrectomy if stenosis

• Previous IC bleed
• Uncontrolled hypertension
• Known vascular structure lesions
• Facial trauma <3 months

• Increasing age
• Hypertension
• Heart disease (especially AF, MI)
• Smoking
• Diabetes
• Hypercholesterolaemia
• Previous stroke/TIA
• Family history

• Mild: Stunned for seconds/minutes, with no amnesia and a possible headache
• Serious: Increased duration of unconsciousness, amnesia, GCS below 5 for >24 hours implies very serious, long recovery

• Cognitive impairment in incomplete recovery
• Post traumatic epilepsy
• Post traumatic syndrome; malasise, headache etc
• Hydrocephalus
• Chronic subdural haematoma

• Airway maintenance/ventilation,
• CT imaging if haematoma/fracture
• Bloods for FBC, biochemistry and clotting
• ICP monitoring

• Sudden, severe occipital heachache
• Vomiting
• Neck stiffness
• Kernig's sign (meningism)
• Coma
• Important to differentiate from migraine

• Bed rest
• Supportive measures, e.g. ventilation
• Hypertension control
• Dexamethasone (reduces cerebral oedema)
• Nimodipine (CCB; prevents vasospasm)

• SOCRATES
• Site: Tension headache quite superficial
• Onset: Age
• Character: throbbing/crushing/pulsatile
• Radiation
• Associated: photophobia/prodromes/nausea
• Timing: Time till maximal symptoms present
• Exac/reliev: Triggers, e.g. posture, cough, alcohol
• Severity: 1-10
• Family history/medication/social history

• Age over 50
• Thunderclap
• Focal/non-focal deficit
• Posture changes (high/low CSF)
• Early morning headaches
• Systemic symptoms
• Seizures/meningism
• Temporal artery tenderness/jaw claudication
• Past history of disease

• GCS
• BP/pulse
• Pyrexia
• Meningism
• Skin rash
• Temporal artery tenderness
• CN tests

• Worse when lying flat, improved when sitting/standing
• Worse in morning
• Persistent nausea/vomiting
• Worse on valsalva (try to breath when airway closed)
• Worse with physical exertion
• Transient visual changes when posture change

• Causes: Mass effect, increases venous pressure, CSF obstruction, ideopathic
• Examination: Papilloedema, CN dysfunction, focal neurological signs

• Characteristics: Headache worse on sitting/standing, relieved by lying flat, due to loss of volume and pressure on CNs, veins/meninges
• Causes: Lumbar punctures, spontaneous intracranial hypotension

• Neurovascular disorder caused by primary dysfunction in brainstem sensory nuclei, with vascular changes occuring due to neural activation
• Pain results from pain-sensitive cranial blood vessels and the trigeminal fibres that innervate them

• Triggers: Hormones, weather, stress, sleep disturbance
• Associated features: With/without aura, pro and post-dromes occur sometimes days from onset

• Lifestyle: Trigger avoidance, e.g. reduce caffeine, regular sleep/meals
• Medical: Simple analgesia, triptans and antiemetics
• Prophylaxis: Beta blockers, tricyclic anti-depressants, anti-epileptics

• Abrupt onset of severe headache which reaches maximal intensity in under 5 minutes (usually less than 30seconds)
• Sub arachnoid haemorrhage unless proven otherwise

• Routine bloods/cultures
• ECG
• Urgent CT (blood visible in most SAHs)
• Lumbar puncture for xanthochromia if CT negative; RBCs degrade in CSF

• CD4 T cell mediated inflammatory process
• Occurs in the white matter of the brain and spinal cord
• Inflammatory cell infiltration, myelin degredation and phagocytosis

• Multiple plaques of demyelination within the brain and spinal cord
• Plaques disseminated in space and time
• Especially found in optic nerves, brainstem, cerebellum, pyramidal tracts
• Focal inflammation
• Permanent axonal destruction

• Optic: Acute, unilateral blurred vision. Pain
• Brainstem: Diplopia, vertigo, nystagmus, numbness, dysarthria/dysphagia
• Cord: Progressive spastic paraparesis, Lhermitte's sign, incontinence, paraesthesia/numbness

• MRI: Multifocal plaques; elliptical bordered lesions with no mass effect
• Lumbar puncture: Oligoclonal IgG and raised CSF mononuclear cells (infiltration)
• VERS: Visual evoked responses, shows optic neuropathy

• Relapsing remitting: >2 neurological disturbances over 2-3 years, with some recovery
• Primary progressive: Only progression, no relapse
• Secondary progressive: Only progression, no relapse, develops from R/R
• Progressive relapsing: Steady progression with superimposed R/R

• Lime disease
• Stroke
• Nerve impingement
• Guillian Barre
• Vitamin deficiency
• Diabetes
• Vasculitides

• Short courses of steroids, e.g. IV methylprednisolone with a PPI
• Only decreases severity/length of relapses
• High dose (1g daily for 3 days

• Beta interferon: Reduces relapse rate and lesion formation
• Immunosuppresants: Azathioprine, cyclophosphamide
• Natalizumab: Anti leucocyte antibody, preventing CNS migration
• Intensive physiotherapy/occupational therapy

• Progressive degeneration of substantia nigra
• Lewy bodies develop; spherical masses which displace cell components (cortical = dementia, brain stem = parkinsons)

• Directly related to pathways which connect to basal ganglia
• Motor: Tremor
• Oculo-motor: Reduced ocular pursuit
• Associative/Limbic: memory loss
• Orbitofrontal: Executive dysfunction

• Progressive degeneration, over months or years
• Motor: Tremor, especially at rest. Rigidity. Bradykinesia. Instability
• Neuropsychiatric: Executive dysfunction, slowed cognitive speed, memory loss, sleep disturbance
• Autonomic: Orthostatic hypotension, hyperhidrosis, constipation

• Parkinsons
• Alzhiemers
• Multiple cerebral infarction
• Drugs
• Supranuclear palsy

• 1 of: Muscular rigidity; pill rolling tremor; postural instability
• 3 of: Unilateral onset; rest tremor; persistent asymmetry; >10yr onset; improvement on levadopa OR levadopa chorea

• Repeated strokes
• Repeated head trauma
• Encephalitis
• More than one affected relative
• Cerebellar signs

• L-DOPA; Dopamine precursor - severe chorea/adverse effects
• Dopamine agonist
• MAO B inhibitors
• COMT inhibitors; later disease - COMT degrades neurotransmitters