Year 2 Neurosensory Pathophysiology CONOR GILLESPIE THIRD YEAR MEDICAL STUDENT HLCGILL2@LIV.AC.UK HTTPS://WWW.LIVERPOOLGUILD.ORG/GROUPS/NEUROSOC
Topics covered Stroke CNS infections Headaches Epilepsy Neuromuscular junction (NMJ) disorders CSF disorders Eye disorders Disorders of motor control (Parkinson's and Huntington's) Disorders of cognition
Topics not covered Basic anatomy Eye disorders (see lecture) Cerebral palsy (MSK block) Pain (see lecture) Psychiatric disorders (but have included them in slides) Hearing and balance (see lecture) Rare neurological conditions (included in slides at end)
Pes Cavus- ‘concave foot’
Charcot-marie tooth disease Neurology and AD inherited disorder, two types (type 1 under Neurosurgery 30, type 2 over 30) illustrated p444 Pathology: Inherited demyelination with thickened ‘onion bulb’ areas of remyelination Progressive demyelinating neuropathy with pes cavus (concave foot) and ‘inverted champagne bottle legs’ Also get wasting of the intrinsic foot and tibial muscles
Headaches Divided into either primary or secondary, or ‘dangerous’ and ‘safe’ Primary: Migraine, Tension headache, cluster headache, ice-pick headache, medication overuse headache, trigeminal neuralgia Secondary: Anything i.e. tumour, haemorrhage, space occupying lesion, infection Dangerous: Subarachnoid haemorrhage (SAH), meningitis, temporal arteritis (Giant cell arteritis) Safe: Everything else
Star fish sign for subarachnoid haemorrhage
Dangerous-Subarachnoid haemorrhage (SAH) Sudden onset (seconds), ‘baseball bat’ or ‘thunderclap’ headache, may be associated Loss of consciousness and focal neurological signs (i.e. stroke) Pathology: Rupture of berry aneurysm (other types of aneurysm?) Causes blood in the subarachnoid space Common vessels: ACOM (40%), MCA (34%), PCOM (20%) Risk factors: Hypertension (main one) and Adult polycystic kidney disease Investigations: CT head (gold standard)- ‘star fish’ sign If not evident on CT use LP BUT MUST WAIT 12hrs- why? Look for Xanthochromia in CSF (bilirubin accumulation) Bilirubin comes from red blood cell breakdown which takes 12 hrs
Neurology Temporal arteritis (Giant cell 2010 headaches arteritis) chapter Vasculitis affecting middle sized arteries Aetiology: W:M 2:1, Much more common over 50 (typically 70s) PC: Headache which develops insidiously, worsened by brushing hair or touching scalp Other key symptoms: Jaw claudication and generalised weakness Can cause inflammation of retinal vessels and blindness if untreated. Investigations: Temporal artery biopsy gold standard, ESR and CRP VERY high on bloods Treat with steroids
Neurology 2010 p74-77 Epilepsy Epilepsy: Two or more seizures Seizure: A paroxysmal neurological event characterised by an abnormal discharge of neurones Seizure specific: Tongue biting, incontinence, prolonged recovery period (vs faint/postural hypotension) 3 categories of seizure: Focal-simple partial (consciousness retained) and complex partial (consciousness lost)- most common Generalised (absence and tonic clonic (second most common) and variants of) Provoked seizures- due to acute physiological abnormalities not epilepsy i.e. Trauma, metabolic abnormalities such as hypoglycaemia, hypocalcaemia, drugs or alcohol) Also status epilepticus
Epilepsy types Focal: from an abnormal discharge from one part of the brain only Generalised: Absence (petit mal)- loss of awareness and a vacant expression for <10 seconds Tonic-clonic (grand mal)- tonic stiffening followed by phase of limb jerking Causes of seizures: lots (Genetic (Lennox-Gastaut syndrome), infection, stroke, autoimmune, tumours, idiopathic (most common)) Status epilepticus-seizures occurring for 30m either continuously or intermittently without recovery EMERGENCY- can cause hypoxia, acidosis, hyperthermia and renal failure Most clinicians don’t treat a single seizure
Motor Neurone disease Motor neurone disease: Progressive degenerative disease of upper and lower motor neurons Get progressive limb weakness with dysarthria (speech difficulty), dysphagia (swallowing difficulty) and tongue weakness Get muscle wasting and fasciculation with brisk reflexes are characteristic with NO sensory involvement Death usually occurs within 3-5 years due to respiratory failure Subtypes: Amyotrophic lateral sclerosis (ALS), Primary lateral sclerosis (only movement affected), spinal muscular atrophy (inherited)
Kumar +Clark p889-890 Myasthenia gravis (MG) Autoimmune disorder of NMJ transmission, characterised by weakness and fatigability of proximal limb and ocular muscles Rare (4 in 100k), women 2:1 affected Pathology- Autoimmune antibodies to the postsynaptic Ach receptor Features: Weakness and fatigability, diplopia and ptosis often weaker at the end of the day, reflexes present but fatigable.
Lambert Eaton myasthaenic syndrome (LEMS) Rare autoimmune syndrome with antibodies against calcium channels of the presynaptic motor neuron channel Flesh and ‘Disordered communication between muscles and nerves’ Bones P264- 267 Paraneoplastic in 40-70% (mainly small cell lung cancer) Weakness is improved on repeated movement as are reflexes (opposite of MG)
Stroke Kumar and Clark p828- 838 Definition: Rapid onset of neurological deficit characterised by cerebral, spinal retinal or focal infarction. Transient ischaemic attack (TIA): Brief episode of neurological dysfunction due to ischaemia not infarction. Difference: TIA is completely reversible, stroke is not 85%: ischaemic (thrombotic, cardio-embolic (AF) 10%: haemorrhagic (Intracranial haemorrhage, SAH) 5%: rare causes
Ischaemic stroke Pathology: Ischaemia followed by infarction and neuronal cell death Fall in ATP with release of glutamate, which opens calcium channels with release of free radicals, leading to inflammatory damage, necrosis and apoptosis. Risk factors: Age, Smoking, AF, Diabetes, hyperlipidaemia, obesity, inactivity, genetics, previous TIA (30% have a stroke 5 years after a TIA)
Stroke clinical features The stroke book 2 nd edition Depends on the artery occluded, all usually sudden onset 69% involve the Middle cerebral artery (MCA), 11% Anterior cerebral artery (ACA) and 9% PCA General: Contralateral hemiparesis or hemiplegia, facial weakness, hemi sensory neglect and loss, aphasia and homonymous hemianopia Anterior circulation: all of general plus Amaurosis fugax (temporary loss of vision in one eye) Posterior circulation: Ataxia, vomiting, vertigo, diplopia MCA: Lots of these, generally face and arm weakness>leg ACA: Leg weakness>arm and face with more frontal lobe defects (apathy or aphasia)
Haemorrhagic stroke Risk factors: Age and hypertension are the main ones Most caused by rupture of small aneurysms Affects the brain tissue itself (parenchyma) so also called intraparenchymal haemorrhage. Features are similar to ischaemic due to sudden onset, occurs in 3 places generally: Basal ganglia (80%), pons (10-15%), cerebellum (5-10%)
Stroke investigations and treatment CT head in acute setting, MRI if CT contraindicated or outside thrombolysis window, Lumbar Puncture If considering a SAH Treat: thrombolysis for ischaemic (not haemorrhage) Occasionally surgery to evacuate blood Thrombolysis: dissolves clots, but must be given within 4.5 hrs of symptom onset and has a high risk of causing bleeds Afterwards: Anti-platelet medication (Aspirin, clopidogrel)
Basal ganglia haemorrhage
Extradural and subdural haematoma Extradural: Rupture of middle meningeal artery from trauma to pterion (weak area formed by bony connections) Lucid interval (temporary recovery before deteriorating) Subdural Often following minor head trauma Old and alcoholics: main risk factors (cortical atrophy stretches blood vessels=more liable to rupture) Rupture of cortical bridging veins not arteries
Hydrocephalus Dilation of the ventricles when an imbalance exists between CSF production and resorption
Types of hydrocephalus Neurology and 3 types: neurosurgery illustrated Obstructive (non-communicating)- obstruction of CSF p374-377 flow within the ventricular system itself Communicating- Obstruction to CSF flow outside the ventricular system i.e. a blockage in the subarachnoid space Normal pressure- Dilation of ventricles but normal CSF pressure on LP Normal pressure classic triad: Dementia, gait ataxia, urinary incontinence
Hydrocephalus Symptoms related to increased ICP (Monroe- Kellie doctrine) Pathology: CSF obstruction, which permeates through the ependymal lining into the periventricular white matter, causing damage Symptoms of raised ICP: Headache often worse in the morning, nausea, vomiting, LOC, false localising signs Treat with Ventriculoperitoneal shunt
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