Selected Notes neuro 1 Flashcards
What is a subarachnoid haemorrhage?
<ul><li>Blood within the subarachnoid space(under arachnoid mater)</li><li><img></img><br></br></li></ul>
Describe the epidemiology of SAH
<ul><li>F>M</li><li>Peak incidence: 40-50 years</li><li>80% without trauma due to a ruptured berry aneurysm</li></ul>
What is the most common cause of a SAH
<ul><li>Head injury</li></ul>
Name some risk factors for developing a Berry aneurysm?
<ul><li>Hypertension</li><li>Adult polycystic kideny disease</li><li>EDS</li><li>Coarctation of the aorta</li></ul>
Name the symptoms of a SAH
<ul><li>Sudden onset 'thunderclap' headache, peaks in intensityin 1-5 minutes</li><li>May have history of previous less severe 'sentinel' headache</li><li>Altered consciousness</li><li>Nausea and vomiting</li><li>Seizures</li><li>Meningism: photophobia and neck stifness</li></ul>
Name the signs of an SAH
<ul><li>Fundoscopy: retinal haemorrhage</li><li>Positive Kernig's/Brudzinksi's sign</li><li>Focal neurological deficits</li></ul>
<div>CN3/4/6-diplopia</div>
<div>Hemiparesis/hemiplegia</div>
What investigations should be done in a patient with a SAH
<ul><li>Non contrast CT head->hyperdense blood in basal cistern</li><li>If normal >6 hours post onset:</li><li>LP if >12 hours post onset: xanthochromia </li><li>CT angiogram to check for aneurysms or vascular abnormalitis</li></ul>
Describe the treatment for an SAH
<ul><li>Oral nimodipine to prevent vasospasm-> ischaemic damage</li><li>Coiling, stenting or clipping of aneurysms: neurosrugery</li></ul>
Name some complications of an SAH
<ul><li>Re-bleeding</li><li>Hydrocephalus</li><li>Vasospasm</li><li>Hyponatraemia->SIADH</li><li>Seizures</li></ul>
Describe the prognosis of a patient with an SAH
<ul><li>If untreated: 50% mortality</li><li>Of those who survive the 1st month: 50% will beocme dependent, 85% recovery in those admitted to neurosurgical unit</li></ul>
Name some predictive factors for the outcome of a patient with an SAH
<ul><li>Age</li><li>Consciousness level on admission</li><li>Amount of blood visible on CT head</li></ul>
Describe the pathophysiology of a patient with a TIA
<ul><li>Transient disruption of blood flow to a specific region of the CNS resulting in ischaemia</li></ul>
Describe the presentaiton of a patient with a TIA
<ul><li>Completely resolves within 24 hours</li><li>Stroke symptoms</li></ul>
<div>Aphasia/dysarthria</div>
<div>Unilateral weakness/sensory loss</div>
<div>Ataxia, vertigo, balance issues</div>
<div>Visual: amaurosis fugax, diplopia, HH</div>
What investigations should be done in a patient with a suspected TIA?
<ul><li>Neuroimaging: MRI(ischaemia, haemorrhage, other pathologies)</li><li>Carotid dopple USS-> atherosclerosis</li><li>Echo: cardiac thrombus</li><li>24hr ECG: AF</li><li>Bloods: glucose, lipid profile, clotting</li></ul>
What is the immediate treatment for a patient with a TIA?
<ul><li>Immediate antithrombotic therapy: aspirin 300mg unless CI</li></ul>
Name some contraindications for aspirin therpay in a patient with a TIA
<ul><li>Bleeding disorder</li><li>Already on aspirin</li></ul>
For a patient with a TIA in the last 7 days, how urgently should they be reviewed by a specialist?
<ul><li><7 days: urgent assessment within 24 hours</li></ul>
For a patient with a TIA over 7 days ago, how urgently should they be reviewed by a specialist
<ul><li>Within 7 days</li></ul>
For a patient with a crescendo TIA or multiple TIAs, how urgently should they be reviewed by a specialist?
<ul><li>Admitted immediately</li><li>Liekly cardioembolic source</li></ul>
Describe the secondary management of TIA
<ul><li>Antiplatelet therapy: clopidogrel</li><li>Lipid moidification: atorvastatin 20-80mg daily</li><li>Carotid endartectomy if severe carotid stenosis</li></ul>
What is an extradural haemorrhage?
<ul><li>Blood collects between the dura mater(outermost meningeal layer) and inner surface of the skull</li></ul>
What is the most common blood vessel implicated in an extradural haemorrhage?
<ul><li>Middle meningeal artery-> thin skull at pterion</li></ul>
<div>Usually arterial</div>
Describe the typical presentaiton of a patient with an extradural haemorrhage
<ol><li>Initial brief los sof consciousness post initial trauma</li><li>Lucid interval(regianed consciousness and apparent recovery)</li><li>Subsequent deterioration of consciousness and headache onset</li></ol>
Describe the pathophysiology of an extradural haemorrhage
<ul><li>Haematoma expands-> uncus of temporal lobe herniates around the tentorium cerebelli-> parasympathetic fibres of CN3 compressed-> fixed and dilated pupil</li></ul>
Name some differentials for a extradural haematoma
<ul><li>Subdural haemorrhage</li><li>SAH</li><li>Intracerebral haemorrhage</li><li>Cerebral contusion</li></ul>
What investigations should be done in a patient with an extradural haematoma?
<ul><li>CT scan: biconvex/lentiform hyperdense collection limited by the suture lines of the skull</li><li>Assess for midline shift/uncal herniation</li><li><img></img><br></br></li></ul>
Describe the management of an extradural haematoma
<ul><li>No neurological deficits-> conservative: supportive therapy and radiological observation</li><li>Definitive: craniotomy and haematoma evacuation</li></ul>
What is a subdural haemorrhage?
<ul><li>Accumulation of venous blood in the potential space between the dura mater and arachnoid mater of the brain</li></ul>
How can subdural haemorrhages be classified?
<ul><li>Acute</li><li>Subacute</li><li>Chronic</li></ul>
Describe the timeline of an acute subdural haemorrhage
<ul><li>Sx develop within 48 hours of injury-> rapid neurological deterioration</li></ul>
Describe the timeline of a subacute subdural haemorrhage
<ul><li>Sx present days-> weeks post injury-> gradual progression of neurological symptoms</li></ul>
Describe the timeline of a chronic subdural haemorrhage
<ul><li>Elderly: weeks-> months</li><li>Might not remember specific head injury</li></ul>
Name some risk factors for developing a subdural haemorrhage
<ul><li>Increasing age</li><li>Anticoag use</li><li>Chronic alcohol use</li><li>Recent trauma</li><li>Infants (shaken baby)</li></ul>
What kind of vessels are implicated in a subdural haemorrhage?
<ul><li>Rupture of bridging veins within subdural space</li></ul>
Describe the typical way in which a patient with a subdural haemorrhage would present?
<ul><li>History of head trauma-> lucid interval-> decline in consciousness</li></ul>
Name some clinical neurological signs you might find in a patient with a subdural haemorrhage
<ul><li>Altered/fluctuating mental status</li><li>Focal neurological deficits</li><li>Headache</li><li>Memory loss</li><li>Cognitive impariment</li><li>Seizures</li><li>Personality changes</li></ul>
Name some possible exam abnormalities in a patient with a subdural haemorrhage
<ul><li>Papilloedema (raised ICP)</li><li>Pupillary changes: unilateral dilated pupil-> CNS compression</li><li>Gait abnormalities</li><li>Hemiparesis/hemiplegia</li><li>Bradycardia, hypertension, irregular respirations (Cushing's triad)</li></ul>
What investigations should be done in a patient with a subdural heamorrhage?
<ul><li>CT scan: screscent shaped, not restricted by suture lines</li><li>Hyperacute(<1hr): isodense</li><li>Acute (<3 days): hyperdense</li><li>Subacute(3d-3 weeks): idosense</li><li>Chronic (>3 weeks): hypodense</li></ul>
<div><img></img><br></br></div>
Describe the management of a patient with a subdural haemorrhage
<ul><li>Conservative: monitor ICP etc</li><li>Acute: decompressive craniotomy</li><li>Chronic: Burr holes</li></ul>
What is an ischaemic stroke?
<ul><li>Sudden onset neurological deficit of vascular aetiology with symptoms lasting >24 hours</li></ul>
Describe the pathophysiology of an ischaemic stroke
<ul><li>Decrease in blood flow-> low O2 and glucose-> energy failure and disruption of cellular ion haemostasis-> exotoxicity, oxidative stress, inflammation and apoptosis-> irreversible neuronal damage</li><li>Can lead to cerebral oedema-> raised ICP-> secondary neuronal damage</li></ul>
Name sone strong risk factors for an ischaemic stroke
<ul><li>Increasing age</li><li>Male</li><li>Family history</li><li>Hypertension</li><li>Smoking</li><li>Diabetes</li><li>AF</li></ul>
Name some weak risk factors for an ischaemic stroke
<ul><li>High cholesterol</li><li>Obesity</li><li>Poor diet</li><li>Oestrogen therapy</li><li>Migraine</li></ul>
How is an ischaemic stroke diagnosed?
<ul><li>Non contrast CT head</li><li>Areas of low density/'hyperdense artery' sign</li></ul>
What is alteplase?
<ul><li>Thrombolytic: tissue plasminogen activator</li></ul>
Describe the secondary prevention of an ischaemic stroke
<ul><li>Clopidogrel 75mg </li><li>Aspiring if clopidogrel CI or not tolerated</li><li>Carotid endartectomy within 7 days if severe carotid stenosis</li><li>Atorvastatin 20-80mg OD</li><li>Smoking cessation and lifestyle advice</li><li>Hypertension treatment and diabetes check</li></ul>
What artery supplies the lateral cerebral cortex?
<ul><li>Middle cerebral artery</li></ul>
What artery supplies the anterior cerebral cortex?
<ul><li>Middle cerebral artery</li></ul>
Describe the symptoms of lateral pontine syndrome and name the implicated artery
<ul><li><div>Ipsilateral:</div><div>-CN3 palsy</div><div>-Vertigo/nystagmus/deafness</div><div>-Poor coordination/tone/balance</div></li><li><div>Anterior inferior cerebellar artery</div></li></ul>
Describe the symptoms of Weber’s syndrome
<ul><li>Ipsilateral CN3 palsy</li><li>Contralateral hemiparesis</li></ul>
Name some cerebellar signs
<ul><li>Nystagmus</li><li>Vertigo</li></ul>
Name some signs of bulbar muscle weakness
<ul><li>Dysphagia </li><li>Dysarthria</li></ul>
What is Horner’s syndrome?
<ul><li>Ptosis</li><li>Miosis</li><li>Anhidrosis</li><li>Damage to sympathetic nerve supply to the eye</li></ul>
What are the criteria for a total anterior circulation stroke?
<div>3/3 of:</div>
<div><ul><li>Unilateral weakness and/or sensory deficit of face, arm and leg</li><li>Homonymous hemianopia</li><li>Higher cerebral dysfunction(dysphasia, visuospatial disorder)</li></ul></div>
What are the criteria for a partial anterior circulation stroke
<div>2/3 of:</div>
<div><ul><li>Unilateral weakness and/or sensory deficit of face, arm and leg</li><li>Homonymous hemianopia</li><li>Higher cerebral dysfunction(dysphasia, visuospatial disorder)</li></ul></div>
What are the criteria for a posterior circulation stroke?
1/5 of:<br></br><ul><li>Cranial nerve palsy and contralateral motor/sensory deficit</li><li>Bilateral motor/sensory deficit</li><li>Conjugate eye movement disorder(horizontal gaze palsy)</li><li>Cerebellar dysfunction (vertigo, nystagmus, ataxia)</li><li>Isolated homonymous hemianopia</li></ul>
What causes a lacunar stroke and which part of the brain does it affect?
<ul><li>Subcortical</li><li>Occurs secondary to small vessel disease</li></ul>
How can a lacunar stroke be differentiated from other strokes?
<ul><li>NO loss of higher cerebral function</li></ul>
What are the criteria for a lacunar stroke?
1/4 of:<br></br><ul><li>Pure sensory stroke</li><li>Pure motor stroke</li><li>Sensori-motor stroke</li><li>Ataxic hemiparesis</li></ul>
What can a CN5 palsy result in?
Trigeminal <br></br><ul><li>Trigeminal neuralgia</li><li>Loss of corneal reflex</li><li>Loss of facial sensation</li><li>Paralysis of mastication muscles</li><li>Deviation of jaw to weak side</li></ul>
What can a CN6 palsy result in?
Abducens<br></br><ul><li>Defective abduction-> hortizontal diplopia</li></ul>
What can a CN7 palsy result in?
Facial<br></br><ul><li>Flaccid paralysis of upper and lower face</li><li>Loss of corneal reflex(efferent)</li><li>Loss of taste</li><li>Hyperacusis</li></ul>
What can a CN8 palsy result in?
Vestibulocochlear<br></br><ul><li>Hearing loss</li><li>Vertigo, nystagmus</li><li>Acoustic neuromas</li></ul>
What can CN9 palsy result in?
Glossopharyngeal<br></br><ul><li>Hypersensitive carotid sinus reflux</li><li>Loss of gag reflex (afferent)</li></ul>
What can a CN10 palsy result in?
Vagus<br></br><ul><li>Uvula deviates away from site of lesion</li><li>Loss of gag reflex(efferent)</li></ul>
What can a CN11 palsy result in?
Accessory<br></br><ul><li>Weakness turning head to contralateral side</li></ul>
What can a CN12 palsy result in?
Hypoglossal<br></br><ul><li>Tongue deviates towards the side of lesion</li></ul>
What is encephalitis?
<ul><li>Inflammation of the brain parenchyma</li></ul>
Describe the epidemiology of encephalitis
<ul><li>Peak: >70 yrs, <1 year</li><li>M:F 1:1</li></ul>
Describe the symptoms of encephalitis
<ul><li>Fever</li><li>Headaches</li><li>Seizures</li><li>Psych sympotms</li><li>Vomiting</li><li>Focal features</li><li>Flu-like prodromal illness</li></ul>
Name some differentials for encephalitis
<ul><li>Hypoglycaemia</li><li>HE</li><li>DKA</li><li>Uremic/drug induced encephalopathy</li></ul>
What investigations should be done in a patient with suspected encephalitis?
<ul><li>CSF testing: lymohocytosis, hgih protein, viral PCR analysis of CSF</li><li>MRI</li><li>EEG</li><li>CT</li></ul>
How is encephalitis treated?
<ul><li>10mg/kg aciclovir TDS for 2 weeks</li><li>Broad spectrum antibiotics e.g. ceftriaxone</li><li>Supportive-seizure management</li></ul>
Name some side effects of aciclovir
<ul><li>GI changes</li><li>Photosensitivity and rashes</li><li>Acute renal failure</li><li>Hepatitis</li></ul>
Describe the prognosis of encephalitis
<ul><li>10-20% mortality of treatment started promptly</li><li>80% mortality if untreated</li></ul>
What is meningitis?
<ul><li>Inflammation of the meninges (dura, arachnoid, pia)</li><li>Can be infective or non infective</li></ul>
Describe the epidemiology of meningitis
<ul><li>Viral(enteroviruses) most common</li><li>Bacterial: associated with increased morbidity and mortality</li><li>Fungal/parasitic: rare except in immunosuppressed</li></ul>
Name the most common bacterial causes of meningitis and the groups they are present in
<ul><li>S.pneumoniae</li><li>N.meningitidis</li><li>H. influenza: infants</li><li>Listeria monocytogenes: Elderly</li></ul>
Name some viral causes of meningitis
<ul><li>Enteroviruses</li><li>Herpes</li><li>VZV</li><li>Measles/rubella</li></ul>
What is the most common fungal cause of meningitis?
<ul><li>Cryptococcus neoformans</li></ul>
Name the parasitic causes of meningitis
<ul><li>Amoeba</li><li>Toxoplasma gardii</li></ul>
Name some non infective causes of meningitis
<ul><li>Malignancies: leukaemia, lymphoma</li><li>Drugs: NSAIDs, trimethoprim</li><li>Systemic inflammatory diseases: Sarcoidosis, SLE, Behcets</li></ul>
Describe the symptoms of meningitis
<ul><li>Headahce</li><li>Fever</li><li>Nausea and vomiting</li><li>Seizures</li><li>Decreased consciousness</li><li>Photophobia</li><li>neck stuffness</li><li>Non blanching petechial/purpuric rash-> DIC</li></ul>
Name some signs in a patient with meningitis
<ul><li>Kernig's sign: Pain and resistance to knee extension</li><li>Brudzinski's sign: passive neck flexion results in involuntary hip and knee flexion</li></ul>
Name some differential diagnoses for meningitis
<ul><li>Encephalitis</li><li>SAH</li><li>Brain abscess</li><li>Sinusitis</li><li>Migraine</li></ul>
What investigations should be done in a patient with suspected meningitis?
<ul><li>Bloods: FBC, CRP, coag screen, cultures, PCR, glucose</li><li>ABG</li><li>CT head</li><li>LP and CSF analysis </li></ul>
Describe the treatment of a patient with suspected meningitis if presenting to a GP
<ul><li>IM benzylpenicillin and urgent hospital transfer</li></ul>
Describe the treatment of a patient with suspected bacterial meningitis in hospital
<ul><li>IV cefotaxima/ceftriaxone and IV dexamethasone</li><li>Add amoxicillin for listeria cover(age extremes)</li></ul>
Describe the treatment of suspected viral meningitis
<ul><li>If enteroviruses: nothing</li><li>If HSV/VZV: aciclovir</li></ul>
What are the prophylaxis recommendations for contacts of meningitis
<ul><li>If in contact 7 days prior to onseet: One off dose of oral ciprofloxacin</li></ul>
Name some complications of meningitis
<ul><li>Sepsis</li><li>DIC</li><li>SIADH</li><li>Seizures</li><li>Waterhouse friedrichsen syndrome</li><li>Delayed: hearing loss, cranial nerve dysfunction, intellectual deficits, ataxia, blindness</li></ul>
What is Waterhouse friedrichsen syndrome?
<ul><li>Adrenal insufficiency caused by intra-abdominal haemorrhage from DIC</li></ul>
Name the causes of meningitis is neonates(0-3 months)
<ul><li>Group B strep</li><li>E.Coli</li><li>Gram negative bacilli</li><li>Listeria</li><li>S.pneumoniae</li></ul>
Name the causes of meningitis in infants(3 months-6 years)
<ul><li>S.pneumoniae</li><li>N.meningitidis</li><li>H. influenzae</li></ul>
Name the causes of meningitis in adults(6-60 years)
<ul><li>S.pneumoniae</li><li>N.meningitidis</li></ul>
Name the causes of meningitis in the elderly (>60yrs)
<ul><li>S.pneumoniae</li><li>N.meningitidis</li><li>Listeria</li><li>Gram negative bacilli</li></ul>
How does S.pneumoniae appear on microbiology?
<ul><li>Gram positive diplococcus in chains</li></ul>
How does Group B strep appear on microbiology?
<ul><li>Gram positive coccus in chains</li></ul>
What age groups is most likely to have meningitis cauased by Group B strep and why?
<ul><li>Neonates</li><li>Colonises in maternal vagina</li></ul>
What age group is most likely to get meningitis from listeria monocytogenes?
<ul><li>Extremes of age, pregnant</li><li>Found in cheese</li></ul>
What does listeria monocytogenes appear like on microbiology?
<ul><li>Gram positive bacillus</li></ul>
What is neurofibromatosis?
<ul><li>Genetic condiiton that causes nerve tumours(neuromas) to develop in the nervous system</li><li>Benign but can cause neurological/structural problems</li></ul>
What are the types of neurofibromatosis and which is more common?
<ul><li>Type 1-more common</li><li>Type 2</li></ul>
What is neurofibromatosis type 1 also called?
<ul><li>Von Recklinghausen's syndrome</li></ul>
Describe the inheritance pattern of neurofibromatosis type 1
<ul><li>Autosomal dominant</li></ul>
Describe the features of neurofibromatosis type 1<br></br><div>CRABBING</div><div><ul><li>C{{c1::afe au lait spots(>15mm)}}</li><li>R{{c2::elative with F1}}</li><li>A{{c3::xillary/inguinal freckles}}</li><li>B{{c4::ony dysplasia-bowing of long bones or sphenoid wing dysplasia}}</li><li>I{{c5::ris hamartomas(Lisch nodules)-yellow/brown spots on iris}}</li><li>N{{c6::eurofibromas(over 2 significant unless more than 1 plexiform)}}</li><li>G{{c7::lioma of optic pathway}}</li></ul></div>
How is neurofibromatosis diagnosed?
<ul><li>Diagnostic criteria and genetic testing</li></ul>
Describe the treatment of neurofibromatosistype 1
<ul><li>Monitor and manage symptoms, treat complications</li></ul>
Name some complications of neurofibromatosis type 1
<ul><li>Malignant peripheral nerve sheath tumours(MPNST)</li><li>Gastrointestinal stromal tumours(GIST)</li><li>Migraines</li><li>Epilepsy</li><li>Hypertension from renal artery stenosis</li><li>Scoliosis</li><li>Brain.spinal tumours</li><li>High cancer risk</li></ul>
What is the inheritance pattern of neurofibromatosis type 2
<ul><li>Autosomal dominant</li></ul>
What is the main symptom/complication of neurofibromatosis type 2?
<ul><li><b>Bilateral</b> acoustic neuromas</li></ul>
What is giant cell arteritis/temporal arteritis?
<ul><li>Vasculitis of unknown cause that affects medium-large sized vessel arteries, especially at the temples</li><li>Overlap with PMR</li></ul>
Describe the epidemiology of giant cell arteritis
<ul><li>Most common primary vasculitis</li><li>>50 years, peaks in 70s</li><li>M:F 1:3</li></ul>
Name some risk factors for giant cell arteritis
<ul><li>Genetics</li><li>Environmental</li><li>Age-fmales</li><li>Sex</li><li>Ethnicity(Mc caucasian-scandinavian)</li></ul>
Describe the presentation of a patient with giant cell arteritis
<ul><li>Usually rapid onset: <1 month</li><li>Temporal headache</li><li>Jaw claudication</li><li>Amaurosis fugax, diplopia</li><li>Tender, palpable temporal artery, scalp tenderness, bruits(rare)</li><li>50% have PMR features(aching, morning proximal limb weakness, lethargy)</li></ul>
What investigations should be done in a patient with giant cell arteritis?
<ul><li>High ESR/CRP</li><li>Normal creatine kinase and EMG</li><li>Temporal artery biopsy-> granulomatous inflammatin and infiltration of giant cells</li><li>Doppler USS: 'halo' sign</li></ul>
Describe the managmeent of giant cell arteritis
<ul><li>Urget high dose steroids: 40-60mg prednisolone OD to prevent blindness</li><li>Then taper(use bisphosphonates/PPI)</li><li>Low dose aspiring to reduce risk of stroke/blindness</li></ul>
Name some complications of giant cell arteritis
<ul><li>Permanent monocular blindness</li><li>Diplopia</li><li>Stroke</li><li>Aortic aneurysms</li></ul>
How can giant cell arteritis result in permanent monocular blindness?
<ul><li>Anterior ischaemic optic neuropathy-> occlusion of posterior ciliary artery-> ischaemia of optic nerve head</li></ul>
How can giant cell arteritis cause diplopia?
<ul><li>Involvement of any paart of oculomotor system(e.g. cranial nerves)</li></ul>
What is Bell’s palsy?
<ul><li>Acute, unilateral, idiopathic facial nerve paralysis</li></ul>
Describe the presentation of Bell’s palsy
<div><ul><li>Acute(not sudden) onset of unilateral LMN facial weakness with NO foreheard sparing</li><li>Post auriicular otalgia(may precede paralysis)</li><li>Hyperacusis</li><li>Nervus intermedius symptoms: altered taste, dry eyes/mouth</li></ul></div>
Name some differential diagnoses for bell’s palsy
<ul><li>Ramsay Hunt syndrome</li><li>Stroke-forehead sparing</li><li>Guillain Barre</li></ul>
What investigations might be done in a patient presenting with suspected Bell’s palsy?
<ul><li>Clinical: rule out other causes/assess extent of damage</li><li>FBC/ESR/CRP/viral serology/lyme serology/otoscopy/EMG/MRI/CT</li></ul>
Describe the management of Bell’s palsy
<ul><li>50mg oral pred OD for 10 days then taper</li><li>Aciclovir in certain patients (e.g. for Ramsay Hunt)</li><li>Supportive: artificial tears/ocular lubricants/eye tape</li></ul>
Describe the prognosis of Bell’s palsy
<ul><li>Complete recovery: 70-80% in weeks-months</li><li>If untreated: 15% have permanent moderate/severe weakness</li></ul>
Name some poor prognostic factors for Bell’s palsy
<ul><li>Older age</li><li>More severe initial facial weakness</li></ul>
What is essential tremore?
<ul><li>Common movement disorder characterised by a rhythmic postural or kinetic tremor primarily affecting the upper extremities</li></ul>
Describe the epidemiology of essential tremor
<ul><li>Commmon</li><li>Increased age: peak 40-50 years</li><li>F:M:1:1</li><li>Family history</li></ul>
Describe the pathophysiology of essential tremor
<ul><li>GABA-ergic dysfunction-> increased activity in cerebellar-thalamic cortical circuit</li></ul>
Describe the features of essential tremor
<ul><li>Postural/kinetic tremor that predominantly affects the upper limbs distally</li><li>Usually bilatera: high frequency: 6-12Hz</li><li>Exacerbated by intentional movements, absent on rest</li><li>Increasing amplitude over time</li><li>Relieved by alcohol</li><li>Exacerbated by anxiety, excitement etc</li><li>Can affect head, lower limbs, voice, tongue, face and trunk</li></ul>
What additional features of essential tremor might prompt further investigation to look for differentials?
<ul><li>Difficulty with tandem gait</li><li>Mild cognitive impairment</li><li>Slight resting tremor alongside action tremor</li></ul>
How is essential tremor diagnosed?
<ul><li>CLinical diagnosis</li><li>bilateral uppper limb action tremor lasting >3 years with no other tremor/neurological signs</li></ul>
Name some differential diagnoses for essential tremor
<ul><li>Parkinson's</li><li>Hyperthyroidism</li><li>Dystonic tremor</li><li>Spasmodic dysphonia</li></ul>
Describe the management of essential tremor
Pharmacological:<br></br><ul><li>Propanolol</li><li>Primidone</li><li>2nd line: gabapentin, topirimate, nimodipine</li></ul><div>Surgical: </div><div><ul><li>DBS</li><li>Botulinum toxin type A injections</li></ul></div>
Describe the prognosis of essential tremor
<ul><li>Typically worsens with increasing age</li><li>Can remain isolated or can spread e..g. to head or voice over years</li><li>Cna cause major disability</li></ul>
What is myasthenia gravis?
<ul><li>Autoimmune disease-> AChR(nicotinic ACH receptor antibodies)</li></ul>
Describe the epidemiology of myasthenia gravis
<ul><li>M:F 1:1</li><li>Bimodal distribution</li><li>Peak incidence in F<40 years and M>60 years</li></ul>
Describe the pathophysiology of myasthenia gravis
85%:<br></br><ul><li>AChR antibodies-> lower ability of ACh to trigger muscle contractioons-> weakness</li><li>Also MuSK(muscle-specific kinase) and LLRP4(low density lipoprotein receptor related protein)-> creation and organisation of AChR-> inadequate AChR</li></ul>
Describe the presentation of a patient with myasethnia gravis
<ul><li>Muscle weakness that worsens with repetitive activity and weakens with rest(typically ocular/bulbar and limb muscles)</li><li>Ptosis</li><li>Diplopia</li><li>Dysarthria</li><li>Dysphagia</li><li>Proximal limb weakness</li><li>EExacerbated by beta blockers, lithium, phenytoin and certain abx</li></ul>
How is myasthenia gravis investigated/diagnosed?
<ul><li>Bedside: ice pack test</li><li>Serology for AChR antibodies, MuSK and LRP4 antibodies</li><li>CT/MRI chest to look for thymomas/thymic hyperplasia</li><li>Edrophonium test</li></ul>
What is the ice pack test for myasthenia gravis?
<div><ul><li>Measure degree of ptosis</li><li>Apply ice pack for a few minutes</li><li>Measure degreee of ptosis again</li><li>Positive if >2mm improvement</li></ul></div>
What is the edrophonium test for myasthenia gravis?
<ul><li>Administer small amount of edrophonium <span>chloride </span><span>(Tensilon)</span></li><li><span>See effects </span></li><li><span>If rapid, transient increase in muscle strenght-> indicative of diagnosis</span></li></ul>
Describe the management of myasthenia gravis
<ul><li>ACh inhibitors: pyridostigmine, neostigmine</li><li>Immunosuppression-> steroids, azathioprine</li><li>Thymectomy</li><li>Rituximab</li><li>Plasma exchange and IVIG</li></ul>
Name some prognostic factors for myasthenia gravis
<ul><li>Age of onset</li><li>Antibody subtype</li><li>Thymus histology</li><li>Response to treatment</li></ul>
Name one complication of myasthenia gravis
<ul><li>Myasthenic crisis</li></ul>
What is a myasthenic crisis?
<ul><li>Life threatening acute worsening of symptoms, often triggered by another illness like a URTI-> can result in respiratory muscle failure</li></ul>
How is a myasthenic crisis treated?
<ul><li>Usual meds</li><li>IVIG and plasmapharesis</li><li>If FVC<=15mL/kg: mechanical ventilation</li></ul>
What is chronic fatigue syndrome?
<ul><li>Chronic disabling condition characterised by profound fatigue and impariment following minimal physical/cognitive effort</li></ul>
Describe the symptoms of chronic fatigue syndrome
<ul><li>Extreme fatigue</li><li>Post-exertional malaise</li><li>Sleep disturbances and unrefreshing sleep</li><li>Cognitive impairment</li><li>Orthostatic intolerance</li><li>Immune/neurological/autonomi/psychiatric manifestations</li></ul>
Name some differential diagnoses for chronic fatigue syndrome
<ul><li>Fibromyalgia</li><li>Depression</li><li>Hypothyroidism</li><li>AI disorders</li></ul>
How is chronic fatigue syndrome diagnosed?
<ul><li>Most clinical-rule out other causes</li></ul>
<div>TFT's, bloods: inflammation, infection, blood cell abnormalities</div>
<div><br></br></div>
<div>Has to last >3 months and significantly decrease ability to engage in activities</div>
Describe the managment of chronic fatigue syndrome
<ul><li>Refere to specialist CSF service if >3 months</li><li>Energy management</li><li>Graded exercise therapy no longer recommended</li><li>Symptoms control-treat other conditions, pain and sleep management</li><li>CBT</li></ul>
What is an acoustic neuroma also known as?
<ul><li>Vestibular schwannoma</li></ul>
What is an acoustic neuroma?
<ul><li>Benign subarachnoid tumour that exerts local pressure on cranial nerve 8</li></ul>
Describe the epidmiology of acoustic neuromas
<ul><li>Rare in UK</li><li>Adults aged 40-60 years</li></ul>
Describe the presentation of acoustic neuroma
<ul><li>Asymmetric/unilateral hearing loss</li><li>Progressive ipsilateral tinnitus</li><li>Sensorineural deaffness</li><li>Larger tumours: raised ICP like focal neurology: CN5/67/8</li><li>Dizziness, headaches, disequilibrium</li></ul>
Name some differential diagnoses for acoustic neuroma
<ul><li>Meniere's disease</li><li>Labyrinthitis</li><li>BPPV</li></ul>
What investigations should be done in a patient with a suspected acoustic neuroma?
<ul><li>Audiometry</li><li>MRI scan of cerebellopontine angle</li></ul>
Describe the management of an acoustic neuroma
<ul><li>Urgetn referral to ENT</li><li>>40mm: surgery</li><li><40mm: 6 monthly annual surveillance scans via MRI</li></ul>
What focal neurology might be seen in a patient with an acoustic neuroma?
<ul><li>CN8: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus</li><li>CN5: absent corneal reflex</li><li>CN7: facial palsy</li></ul>
What is Meniere’s disease?
<ul><li>Inner ear disorder caused by increased fluid pressure in the endolymphatic spaces of the membranous labyrinth</li></ul>
Describe the epidemiology of Meniere’s disease?
<ul><li>30-60 years</li><li>Predominantly unilateral</li></ul>
Describe the presentation of meniere’s disease
<ul><li>Sudden attacks of paroxysmal vertigo</li><li>Attacks last minutes to hours</li><li>Associated deafness</li><li>Tinnitus</li><li>Attacks often occur in clusters with period of remission where funciton is recovered</li><li>Can cause nystagmus and positive Romberg's test</li><li>Can be very disabling-> bedbound with nausea, vomiting and fluctuating hearing</li></ul>
Name some differential diagnoses for meniere’s disease
<ul><li>Vestibular neuritis</li><li>Labyrinthitis</li><li>BPPV</li></ul>
What investigations are used to diagnose meniere’s disease?
<ul><li>Clinical evaluation</li><li>Audiometric testing</li><li>Imaging/other tests may be used ot rule out other potential causes of symptoms</li></ul>
Describe the management of meniere’s disease
<ul><li>ENT assessment</li><li>Prophylactic use of betahistine to reduce frequenct</li><li>Acute: prochlorperazine</li><li>Diuretics-> reduce endolymphatic fluid(only prescribed by specialists)</li><li>Low salt diets can help rpevent attacks</li><li>DVLA: no driving until good control of sx</li></ul>
Describe the natural history of Meniere’s disease
<ul><li>Sympotms resolve in most patients after 10-15 years</li><li>Majority of patients left with a degree of hearing loss</li><li>Psychological distress common</li></ul>
What is trigeminal neuralgia?
<ul><li>Chronic pain condition characterised by severe sudden and brief bouts of shooting/stabbing pain that follow the distribution of one or more divisions of the trigeminal nerve, affecting the patients facial region</li></ul>
Describe the epidemiology of trigeminal neuralgia
<ul><li>>50yrs</li><li>F>M</li></ul>
Describe the presentation of a patient with trigeminal neuralgia
<ul><li>Unilateral facial pain that is sudden, severe and brief</li><li>Pain is shooting/stabbing</li><li>Triggered by lightly touching affected side of face, eating, or wind blowing</li><li>Neuro exam is typically normal</li></ul>
Name some differential diagnoses for trigeminal neuralgia
<ul><li>Post herpetic neuralgia</li><li>Temperomandibular joint disorders</li><li>Giant cell arteritis</li><li>Cluster headache</li></ul>
How is trigeminal neuralgia diagnosed?
<ul><li>Mostly clinical</li><li>MRI or other neuroimaging to rule out secondary causes</li></ul>
Describe the management of trigeminal neuralgia
Medical:<br></br><ol><li>Carbamazepine</li><li>Phenytoin</li><li>Lamotrigine</li><li>Gabapentin</li></ol><div>Surgical:</div><div><ul><li>Microvascular decompression-remove/relocate vessels</li><li>Treat underlying cause like AVM/tumour</li><li>Alcohol/glycerol injections</li></ul><div><br></br></div></div><div>Failure to respond to treatment/atypical: refer to neuro</div>
Name some red flag symptoms for trigeminal neuralgia
<ul><li>Sensory changes</li><li>Deafness</li><li>Pain only in ophthalmic division(eye socket, forehead and nose) or bilaterally</li><li>Optic neuritis</li><li>FHx of MS</li><li><40 yrs</li></ul>
What is bulbar palsy?
<ul><li>Subtype of LMN lesion impacting the 9/10/12th cranial nerves</li></ul>
Name the major causes of bulbar palsy
<ul><li>Motor neurone disease-mc</li><li>Myasthenia gravis</li><li>Guillain-barre</li><li>Brainstem stroke-Wallenberg's/lateral medullary syndrome</li><li>Syringobulbia</li></ul>
Describe the signs and symptoms of bulbar palsy
<ul><li>Dysarthria and dysphagia</li><li>Absent/normal jaw jerk reflex</li><li>Absent gag reflex</li><li>Flaccid, fasciculating tongue</li><li>Nasal speech, often described as 'quiet'</li><li>Additional signs suggestive of underlying cause(e.g. limb fasciculations: MND)</li></ul>
Name some differentials for bulbar palsy
<ul><li>Pseudobulbar palsy</li><li>Brainstem tumour</li><li>MS</li><li>Polymyositis and dermatomyositis</li></ul>
What investigations should be done in a patient with bulbar palsy?
<ul><li>Neuro exam</li><li>EMG and nerve conduction studies:MND/mysthenia gravis</li><li>Bloods: FBC, electrolytes, CK, autoantibody screening</li><li>MRI-lesions in brainstem</li><li>LP: rule out infections/AI causes</li></ul>
How is bulbar palsy managed?
<ul><li>Speech and swallowing therapy-manage dysarthria and dysphagia</li><li>Nutritional support</li><li>Treat underlying cause</li></ul>
How can Horner’s syndrome be characterised?
<ul><li>Pre-ganglionic</li><li>Post-ganglionic</li><li>Central</li></ul>
<div>Dependent on locatoin of sympathetic nerve interruption</div>
Name some causes of Horner’s syndrome
<ul><li>Pancoast tumour: pre-ganglionic</li><li>Stroke-central</li><li>Carotid artery dissection: post-ganglionic</li><li>Trauma, tumours, surgery-central</li></ul>
What is a pancoast tumour and how can it case Horner’s syndrome?
<ul><li>Non-small cell lung carcinoma</li><li>Located at superior sulcus of lung affects lower roots of brachial plexus anf sympathetic chain</li></ul>
How do patients with Horner’s syndrome typically present?
<ul><li>Ptosis-dropping of upper eyelid</li><li>Miosis-constriction of pupil</li><li>Anhidrosis</li><li>Enophthlamos-eye may appear sunken</li><li>Heterochromia-eye colour may change, more common in congenital Horner's syndrome</li><li><img></img><br></br></li></ul>
Name some differential diagnoses for Horner’s syndrome
<ul><li>Oculomotor nerve palsy-will also have ophthalmoplegia</li><li>Myasthenia gravis</li><li>Bell's palsy</li></ul>
What investigations might be done in a patient presenting with Horner’s syndrome?
<ul><li>Imaging: MRI/CT head neck and chest to ID structural causes</li><li>Bloods: assess for diabetes or AI disorders</li></ul>
<div>Pharmacological pupil testing to confirm diagnosis and differentiate between pre- and post-ganglionic lesions</div>
Describe the management of Horner’s syndrome
<ul><li>Treat underlying cause</li><li>If no casue identified, observatoin and regular follow up</li><li>Cosemtic interventions for ptosis or miosis may be considered</li></ul>
What is Guillain Barre syndrome?
<div><ul><li>Ascending inflammatory demyelinating polyneuropathy-> acute onset of bilateral and roughly symmetric limb weakness</li></ul></div>
How do patients with Guillan Barre present?
<ul><li>Progressive ascending symmetrical limb weakness-> lower limbs first</li><li>Low back pain from radiculopathy</li><li>Paraesthesia</li><li>LMN signs in lower limbs: hypotonia, flaccid paralysis, areflexia</li><li>Cranial nerve signs: opthlamoplegia, facial nerve palsy, bulbar palsy</li><li>Potential autonomic dysfunction</li><li>Potential respiratory muscle involvement</li></ul>
Name some variants of Guillaim Barre syndrome
<ul><li>Parapetic</li><li>Miller-Fischer</li><li>Pure motor</li><li>Bilateral facial palsy with paraesthesias</li><li>Pharyngeal brachial cervical weakness</li><li>Bickerstaff's brainstem encephalitis</li></ul>
Name some differential diagnoses for Guillain Barre
<ul><li>Vascular: strokes</li><li>Infective/inflammatory: polio, lyme, CMV, TB, HIV, CIDP, myastehnia gravis</li><li>Spinal cord compression</li><li>Metabolic-porphyria, electrolyte abnormalitis</li></ul>
What investigations might be done in a patient with suspected Guillain Barre?
<ul><li>Monitoring of FVC for respiratory muscle involvement</li><li>Serological: anti ganglioside antibodies</li><li>LP: albuminocytological dissociation</li><li>Nerve conduction studies: prolongation or loss of the F wave</li><li>ID underlying cuase: stool cultures, serology, CSF virology</li></ul>
What might be seen on an LP of a patient with Guillain barre?
<ul><li>albuminocytological dissociation</li><li>Increased albumin without corresponding increase in white blood cells</li></ul>
How is Guillain Barre managed?
<ul><li>Regular FVC monitoring-can rapidly deteriorate</li><li>VTW prophylaxis: TEDS and LMWH</li><li>Analgesia if needed</li><li>Manage complications: arrhythmias, autonomic dysfunction</li><li>Enteral feeding if unsafe swallow</li></ul>
<div>If significant disability:</div>
<div><ul><li>IVIG for 5 days</li><li>Plasmapharesis(more side effects that IVIG)</li></ul></div>
What is the prognosis of Guillain Barre syndrome
<ul><li>Mostly full recovery</li><li>Can have residual weakness or fatigue</li></ul>
Give some prognostic factors for Guillain Barre
<ul><li>Speed of onset</li><li>Severity</li><li>Age</li><li>Presence of preceding diarrhoeal illness</li></ul>
What is Miller Fisher syndrome?
<ul><li>Variant of GBS</li><li>Ophthalmoplegia, areflexia and atacis(eye muscles affected first-descending paralysis)</li><li>Anti GQ1b antibodies in 90%</li></ul>
Describe the pathophysiology of Guillain Barre syndrome
<ul><li>Cross reaction of antibodies with gangliosides in the peripheral nervous system</li><li>Correlation between anti-ganglioside antibody and clinical features</li><li>Anti-GM1 antibodies </li></ul>
What is Huntington’s disease?
<ul><li>Genetic disorder that causes progressive breakdown of nerve cells in brain leading to motor, cognitive and psychiatric abnormalitis</li></ul>
Describe the epidemiology of Huntington’s disease
<ul><li>Most common neurodegenerative disorder</li></ul>
What is meant by ‘anticipation’ with regards to genetics in Huntington’s disease
<ul><li>Number of CAG repeats directly correlated with disease severity and age of onset</li><li>Symptoms present earlier in excessive generations due to increase in number of repeats</li></ul>
Describe the presentation of a patient with Huntington’s disease
<ul><li>Choreoathetosis: unpredictable flowing and writhing movements</li><li>Cognitive impairment: dementia</li><li>Psychiatric abnormalitis: depression, irritability apathya nd sometimes psychosis</li></ul>
<div><br></br></div>
<div>Usually over age 35YRS</div>
<div>Dystonia</div>
<div>Saccadic eye movements</div>
Give some differential diagnoses for Huntington’s disease
<ul><li>Parkinson's</li><li>Wilson's disease</li><li>Huntington's disease like disorders</li><li>Neuroacathocytosis syndromes</li></ul>
How is Huntington’s Disease diagnosed?
<ul><li>MRI/CT: loss of striatal volume and enlarged frontal horn of lateral ventricles</li><li>Genetics: including for at risk family members</li></ul>
How is Huntington’s disease managed?
<ul><li>Chorea management; tetrabenazine</li><li>Depression: SSRI</li><li>Psychosis: atypical antipsychotics</li><li>Supportive: physical and emotional support from MDT</li></ul>
What is the prognosis for Huntington’s Disease?
<ul><li>Decline in physical and cognitive abilitys</li><li>Detah usually due to complications related to physical decline like pneumonia</li><li>Suicide second mc cause of death</li></ul>
Describe the pathophysiology of Huntington’s disease
<ul><li>Autosomal dominant mutaiton results in degeneration of cholinergic and GABAergic neurons in striatum of basal ganglia</li></ul>
What is a seizure?
<ul><li>Transient occurences of signs and symptoms due to abnormal excessive or synchronous neuronal activity in the brain</li></ul>
Name some differential diagnoses for epilepsy
<ul><li>Syncope</li><li>TIA</li><li>Migraines</li><li>Panic disorder</li><li>Non epileptic attack disorder</li></ul>
What investigations might be done in a patient with a seizure?
<ul><li>History including collateral and neuro exam</li><li>Imaging like CT/MRI</li><li>EEG</li><li>Might consider LP, bloods, advanced imaging depending on background</li></ul>
Name some localising features of temporal lobe seizures
<ul><li>Can occur with/without impairment of consciousness or awareness</li><li>Usually has an aura: rising epigastric sensation, psychic phenomena</li><li>Automatisms: lip smacking, grabbing, plucking</li></ul>
Name some localising features of frontal lobe seizures
Frontal lobe-motor<br></br><ul><li>Head/leg movements</li><li>Posturing</li><li>Post-ictal weakness</li><li>Jacksonian march</li></ul>
Name some localising features of parietal lobe seizures
Parietal lobe-sensory<br></br><ul><li>Paraesthesia</li></ul>
Name some localising features of occipital lobe seizures
Occipital-visual<br></br><ul><li>Floaters/flashers</li></ul>
What is the new seizure classification based on?
<ol><li>Where seizure started in the brain</li><li>Level of awareness during seizure</li><li>Other features</li></ol>
What are focal seizures?
<ul><li>Previously: partial seizures</li><li>Start in a specific area on one side of the brain</li><li>Level of awareness can vary</li></ul>
How can focal seizures be further classified?
Based on awareness:<br></br><ul><li>Focal aware(simple partial)</li><li>Focal impaired awareness(complex partial)</li></ul>
Describe the features of a generalised seizure
<ul><li>Involve both sides of the brain at onset</li><li>Consciousness lost immediately</li><li>Can be further divided into tonic-clonic and absence etc</li></ul>
What is Jacksonian March?
<ul><li>Type of focal motor seizure that progressively 'marches' through adjacent areas of brain</li><li>Typically starts in hands and face then speards to other muscle group(hands, arm, shoulder, face)</li><li>Seizure may progress into generalised tonic clonic seizure</li><li>Often associated with structural brain lesions</li></ul>
What is Todd’s paresis?
<ul><li>Temporary postictal weakness or paralysis following a seizure</li><li>Usually lasts minutes to hours but can last up to 48 hours</li><li>Usually unilateral but can be bilateral</li><li>Transient so patient will recover following resolution of postictal state</li></ul>
Describe the treatment of generalised tonic-clonic seizures
<ul><li>Males: sodium valproate</li><li>Females: lamotrigine or levetiracetam</li></ul>
Describe the management of focal seizures
<ol><li>Lamotrigine/levetiracetam</li><li>Carbamazepine</li></ol>
<div><span>foCaL = Carbamazepine + lamotrigine/levetiracetam</span><br></br><span>generaLiSed = lamotrigine/levetiracetam + sodium valproate</span><br></br><span>abSEnce= sodium valproate + ethosuximide</span><br></br></div>
Describe the management of absence seizures
<ol><li>Ethosuximide</li><li>Lamotrigine/levetiracetam(sodium valproate in males)</li></ol>
<div><span>foCaL = Carbamazepine + lamotrigine/levetiracetam</span><br></br><span>generaLiSed = lamotrigine/levetiracetam + sodium valproate</span><br></br><span>abSEnce= sodium valproate + ethosuximide</span><br></br></div>
Describe the management of myoclonic seizures
<ul><li>Males: sodium valproate</li><li>Females: levetiracetam</li></ul>
<div><span>foCaL = Carbamazepine + lamotrigine/levetiracetam</span><br></br><span>generaLiSed = lamotrigine/levetiracetam + sodium valproate</span><br></br><span>abSEnce= sodium valproate + ethosuximide</span><br></br></div>
Describe the management of tonic/atonic seizures
<ul><li>Males: sodium valproate</li><li>Females: lamotrigine</li></ul>
<div><span>foCaL = Carbamazepine + lamotrigine/levetiracetam</span><br></br><span>generaLiSed = lamotrigine/levetiracetam + sodium valproate</span><br></br><span>abSEnce= sodium valproate + ethosuximide</span><br></br></div>
What is sodium valproate associated with when used in pregnancy?
<ul><li>Neural tube defects</li></ul>
What is phenytoin associated with when used in pregnancy?
<ul><li>Cleft palate</li></ul>
Name some complications of epilepsy
<ul><li>Status epilepticus</li><li>Psychiatric complications-> increased risk of depression adn epilepsy</li><li>Sudden unexpected death in epilepsy(SUDEP)</li></ul>
Name some side effects of topirimate
<ul><li>Abdo pain</li><li>Cognitive impairment</li><li>Confusion</li><li>Muscle spams</li><li>mood changes</li><li>n+v</li><li>trmor</li><li>weight loss</li></ul>
Name some side effects of lamotrigine
<ul><li>blurred vision</li><li>arthralgia</li><li>ataxia</li><li>diarrhoea</li><li>dizziness</li><li>headache</li><li>insomnia</li><li>rash</li><li>tremor</li></ul>
Name some side effects of carbamazepine
<ul><li>ataxia</li><li>blood disorders</li><li>blurred vision</li><li>fatigue</li><li>hyponatraemia</li></ul>
name some side effects of sodium valproate
<ul><li>ataxia</li><li>anaemia</li><li>confusion</li><li>gastric irritation</li><li>haemorrhage</li><li>hyponatraemia</li><li>tremor</li><li>weight gain</li></ul>
name some side effects of phenytoin
<ul><li>acne</li><li>anorexia</li><li>constipation</li><li>hirsutism</li><li>insomnia</li><li>rash]tremor</li></ul>
What are the DVLA rules with regards to epilepsy?
<ul><li>Car/motorbike: 1 seizure: 6 months, >1: 1 year</li><li>If following change to medication have to wait 6 months</li><li>bus/coach lorry: 5 years after 1 off seizure. If >1 seizure: 10 seizure freee years</li></ul>
What is status epilepticus?
<ul><li>Seizure lasting >5 minutes OR</li><li>Multiple seizures over 5 minutes without fully regaining consciousness between </li></ul>
Describe the management of status epilepticus
<ul><li>Buccal midazolam or rectal diazepam-can repeat </li><li>If IV access: IV lorazepam repeated after 10-20 minutes</li><li>MAX 2 dose benxos</li><li>2nd line: levitiracetam, phenytoin, sodium valproate</li></ul>
Refractory status(20-90 minutes)-general anaesthesia<br></br><ul><li>Propofol</li><li>midazolam infusion</li><li>thiopental sodium</li></ul>
What investigations might be done in a patient with status epilepticus?
<ul><li>ABG</li><li>Bloods: FBC, U&E, LFT, CRP, clotting, bone profile</li><li>Toxicologyc screen</li><li>Anti epileptic drug</li><li>Imagine to determien cause: CT/MRI, LP</li></ul>
Describe the epidemiology of MS
<ul><li>Females: 2.3:1</li><li>Average onset 30yrs</li></ul>
Describe the symptoms of MS
Visual:<br></br><ul><li>Optic neuritis</li><li>Optic atrophy</li><li>Uhtoff’s phenomenon: worsening of vision following rise in body temperature</li><li>Internuclear ophthalmoplegia</li></ul><div>Sensory:</div><div><ul><li>Paraesthesia</li><li>Lhermittes phenomenon: paraesthesia in limbs on neck flexion</li></ul><div>Motor:</div></div><div><ul><li>Spastic weakness</li></ul><div>Cerebellar:</div></div><div><ul><li>Ataxia</li><li>Tremor</li></ul><div>Others:</div></div><div><ul><li>Urinary incontinence</li><li>Sexual dysfunction</li></ul></div>
How can MS be classified?
<ul><li>Relapsing remitting-> may become secondary progressive</li><li>Primary progressive</li></ul>
Name some differentials for MS
<ul><li>SLE</li><li>Lyme disease</li><li>Neurosarcoidosis</li><li>Vitamin B12 deficiency</li></ul>
How is MS diagnosed?
<ul><li>MRI showing >2 periventricular white matter lesions disseminated in time and space</li><li>Oligoclonal bands in CSF electrophoresis</li></ul>
What criteria is used to diagnose MS?
<ul><li>McDonald criteria</li></ul>
Describe the long term management of MS
<ul><li>Natalizumab-biologics</li><li>Ocrelizumab</li><li>Beta-interferon-injectable</li></ul>
<div>Symptomatice therapies:</div>
<div><ul><li>Physio</li><li>Baclofen and botox for spasticity</li><li>Anticholinergics for bladder dysfunction</li><li>Sildenafil for ED</li></ul></div>
Name some risk factors that might suggest a worse prognosis for a patient with MS
<ul><li>Older age at onset</li><li>Make</li><li>Primary progressive</li><li>High relapse rate</li><li>Rapid accumulation of disability</li><li>Comorbid conditions</li><li>Smoking</li></ul>
What is normal pressure hydrocephalus?
<ul><li>Neurological disorder where CSF accumulates in the ventricles causing them to enlarge</li></ul>
Describe the epidemiology of normal pressure hydrocephalus
<ul><li>More common in older adults</li><li>Considered a significant cause of reversible dementia </li></ul>
How can diabetic peripheral neuropathy be categorised?
<ul><li>Distal symmetrical sensory neuropathy</li><li>Small fibre predominant neuropathy</li><li>Diabetic amyotrophy</li><li>Mononeuritis multiples</li><li>Autonomic neruopathy</li></ul>
What is the most common subtype of diabetic peripheral neuropathy
<ul><li>Distal symmetrical sensory neuropathy</li></ul>
Describe the features of distal symmetrical sensory neuropathy
<ul><li>Most common form of diabetic peripheral neuropathy</li><li>Results from loss of large sensory fibres</li><li>'glove and stocking' distribution affecting touch, vibration and proprioception</li></ul>
Describe the features of small fibre predominant neuropathy
<ul><li>Loss of small sensory fibres</li><li>Loss of pain and temperature sensation in 'glove and stocking' distribution accompanied by epsiodes of burning pain</li></ul>
Describe the features of diabetic amyotrophy
<ul><li>Originates from inflammation of the lumbrosacral plexus or cervical plexus</li><li>Characterised by severe pain around thighs and hips and proximal weakness</li></ul>
Describe the features of mononeuritis multiplex
<ul><li>Painful</li><li>Neuropathies involving >=2 distinct peripheral nerves</li></ul>
Describe the features of autonomic neuropathy
<ul><li>Postural hypotension</li><li>Gatroparesis</li><li>Constipation</li><li>Urinary retention</li><li>Arrhythmias</li><li>Erectile dysfunction</li></ul>
Name some differentials for diabetic peripheral neuropathy
<ul><li>Vitamin B12 deficiency</li><li>Alcohol induced peripheral neuropathy</li><li>CIDP</li><li>Hypothyroidism</li></ul>
What investigations might be done in a patient with diabetic peripheral neuropathy?
<ul><li>Neuro exam</li><li>Nerve conduction tests</li><li>Bloods-HbA1c, B12, TFTs, LFTs</li></ul>
Name some complicaitons of diabetic peripheral neuropathy
<ul><li>Foot ulcers due to loss of sensation</li><li>Autonomic neuropathy-> cardiac, GI and GU disturbances</li></ul>
Describe the management of diabetic peripheral neuropathy
<ul><li>Control of blood glucose levels and treat complications(foot ulcers etc)</li><li>1)amitriptyline, duloxetine, gabapentin, pregabalin</li><li>2)Try other drugs from first line if one fails</li><li>3)Tramadol as 'rescue therapy' for exacerbations</li><li>Topical capsaicin if localised</li></ul>
What is Charcot neuropathy?
<ul><li>Chronic progressive condition characterised by painful or painless bone and joint destruction in limbs that have lost sensory innervation</li></ul>
What are the signs and symptoms of Charcot arthropathy?
6D’s<br></br><ul><li>Destruciton of bone and joint</li><li>Deformity</li><li>Degeneration</li><li>Dense bones</li><li>Debris of bone fragments</li><li>Dislocation</li></ul>
Name some differentials for charcot arthropathy
<ul><li>Osteomyelitis-> important to rule out</li></ul>
What investigations are used to diagnose charcot arthropathy
<ul><li>Clinical dx mostly</li><li>X-rays 1st line imaging: bone destruction, debris, sclerosis and dislocation</li><li>MRI if ostemyelitis suspected</li></ul>
How is charcot arthropathy managed?
<ul><li>Conservative: lifestyle, footwear, orthotics</li><li>Medications: bisphosphonates, gabapentin</li><li>Surgical: resection of bony prominences, amputation if severe</li></ul>
Describe the symptoms of cerebellar dysfunction
DANISH<br></br><ul><li>Dysdiadochokinesia</li><li>Ataxia</li><li>Nystagmus</li><li>Intention tremor</li><li>Slurred speech</li><li>Hypotonia</li></ul>
Name the causes of cerebellar syndrome
PASTRIES<br></br><ul><li>Paraneoplastic syndrome</li><li>Alcohol</li><li>Sclerosis-MS</li><li>Tumours</li><li>Rare-Friedreich’s ataxia</li><li>Iatrogenic-phenytoin, carbamazepine</li><li>Endocrine/metabolic: hypothyroidism/Wilson’s</li><li>Stroke</li></ul>
How is cerebellar dysfunction investigated/diagnosed?
<ul><li>CT/MRI: ID stroke, tumours, trauma</li><li>Serologu: infectious/inflammatory causes</li><li>LP: infection, inflammation, malignancy</li><li>Genetics-hereditary</li></ul>
How is cerebellar dysfunction managed?
<ul><li>Treat underlying cause</li><li>Surgery/meds as required</li><li>Lifestyle-alcohol etc</li><li>Rehab: OT, physio etc</li></ul>
What is Parkinson’s disease?
<ul><li>Chronic progressive neurological condition</li></ul>
Describe the epidemiology of parkinson’s disease
<ul><li>2nd mc neurodegenerative disorder after Alzheimer's</li><li>>65yrs</li><li>M>F</li></ul>
Describe the pathophysiology of Parkinson’s disease
<ul><li>Accumulation of Lewy bodies in the substantia nigra of the basal ganglia-> neuronal cell death of dopaminergic cells</li></ul>
What are lewy bodies?
<ul><li>intracellular inclusions composed mostly of misfolded alpha synuclein</li></ul>
What are the components of the basal ganglia?
<ul><li>Striatum-> dorsal and ventral</li><li>Globus pallidus</li><li>Thalamus</li><li>Substantia nigra</li><li>Subthalamic nucleus</li></ul>
How does parkinson’s affect the direct movement pathway?
<ul><li>Decreased levels of dopamine</li><li>Decreases direct pathway</li><li>Can't initiate increased movement-> decreased movement</li></ul>
Describe the indirect motor pathway in the substantia nigra
<ul><li>Inhibitory</li><li>Decreases thalamus activity</li><li>Decreases movement</li></ul>
How does parkinson’s affect the indirect movement pathway?
<ul><li>Less dopamine</li><li>Increases indirect pathway</li><li>Can't prevent excessive movement pathway</li><li>Decreases movement</li></ul>
Name some risk factors for Parkinson’s disease
<ul><li>Family hx-especially when onset <50yrs</li><li>Previous head injury</li></ul>
Name some protective factors for Parkinson’s disease
<ul><li>Smoking-> including past smoking</li><li>Caffeine intake</li><li>Physical activity</li></ul>
What is the triad of symptoms associated with Parkinson’s disease?
Tremor<br></br>Muscle rigidity<br></br>Bradykinesia
Describe the tremor associated with Parkinson’s disease
<ul><li>Resting tremor</li><li>'pill rolling'</li><li>Asymmetrical</li><li>3-5Hz</li></ul>
How does bradykinesia present in a patient with Parkinson’s disease
<ul><li>Parkinsonian gait-> shuffling, slowness of movement especially on initiation and turning</li></ul>
How does muscle rigidity present in Parkinson’s disease?
<ul><li>'Cogwheel rigidity'</li><li>Decreased arm swing</li><li>Stooped posture</li></ul>
Name some motor symptoms of Parkinson’s disease
Triad of:<br></br><ul><li>Tremor</li><li>Bradykinesia</li><li>Muscle rigidity</li></ul><div>Also:</div><div><ul><li>Postural instability-> increased falls</li><li>Hypomimic facies</li><li>Hypokinetic dysarthria, speech impairment, dysphagia</li><li>Micrographia</li></ul></div>
Name some non motor symptoms of Parkinson’s disease
<ul><li>Autonomic dysfunction</li><li>Sleep dysfunction(REM behavioural disorder)</li><li>Olfactory loss</li><li>Psychiatric-> depression, anxiety, hallucinations, psychotic episodes, paranoid delusions</li></ul>
How is Parkinson’s disease diagnosed?
<ul><li>Most clinical and positive response to treatment trials(excluded by absolute failure to respond to 1-1.5g levodopa daily)</li></ul>
<div>If doubt:</div>
<ul><li>MRI head-absence of swallow tail sign</li><li>Dopamine transporter scan</li></ul>
Name some differentials for Parkinson’s disease
<ul><li>Essential tremor</li><li>Multiple system atrophy</li><li>Lewy body dementia</li></ul>
How is essential tremor differentiated from Parkinson’s disease tremor?
Essential tremor vs Parkinson’s<br></br><ul><li>Symmetrical bs asymmetrical</li><li>6-12Hz vs 3-6hz</li><li>Improves at rest vs worse at rest</li><li>Worse with intentional movements vs improves with movement</li><li>Improves with alcohol vs no changes with alcohol</li></ul><div>Parkinson’s: additional parkinson’s features</div>
Name some complications of Parkinson’s disease
<ul><li>Autonomic dysfunction</li><li>Recurrent falls</li><li>Cognitive imapirment</li></ul>
What is the 1st line treatment for Parkinson’s disease
<ul><li>Levodopa</li></ul>
How does levodopa work for Parkinson’s disease
<ul><li>Dopaminergic</li><li>Precursor to dopamine-> converted in CNS and periphery</li></ul>
What drug is levodopa often dosed with for treating Parkinson’s disease patients and why?
<ul><li>Carbidopa</li><li>Decreases conversion of levodopa in periphery-> increases CNS availability and decreases peripheral side effects</li></ul>
Name some peripheral side effects of levodopa
<ul><li>Postural hypotension</li><li>Nausea and vomiting</li></ul>
Name some central side effects of levodopa
<ul><li>Hallucinations</li><li>Confusion</li><li>Dyskinesia</li><li>Psychosis</li></ul>
What are 2 problems with long term levodopa therapy other than side effects?
<ul><li>End of dose effect</li><li>On and off phenomenon</li></ul>
What is the end of dose effect in levodopa therapy?
<ul><li>AKA wearing off effect</li><li>Medications effect wears off as next dose is due so symptoms get worse</li></ul>
What is the on and off phenomenon in patients with levodopa therapy
<ul><li>'On' periods where medication works well and 'off' periods where medication doesn't work as well</li><li>As it progresses, duration of 'on' periods can shorten and 'off' periods becomme more frequent</li></ul>
Give some examples of MAO-B inhibitors and how they can help in Parkinson’s disease
<ul><li>Rasagiline and selegilin</li><li>Decrease dopamine breakdwon peripherally so increase central uptake</li></ul>
What is an important potential complication of using MAO-B inhibitors?
<ul><li>Can cause serotonin syndrome</li></ul>
Give some examples of COMT inhibitors and how they are used in Parkinson’s disease treatment
<ul><li>Entacapone and tolcapone</li><li>Extend use of levodopa-> good for wearing off effect of levodopa</li></ul>
Give some examples of dopamine agonists and how they are useful for Parkinson’s disease
<ul><li>ropinirole</li><li>rotigotine</li><li>apomorphine-most potent</li><li>mimic dopamine</li></ul>
What is an important side effect of apomorphine?
<ul><li>Haemolytic anaemia</li></ul>
What is<b> </b>hypoxic-ischaemic encephalopathy?
<ul><li>Neurological condition resulting form inadequate cerebral oxygen supply</li></ul>
Name some situations in which hypoxic-ischaemic encephalopathy can occur
<ul><li>Neonates: pperinatal asphyxia</li><li>Adults: secondary to cardiac arrest/severe systemic hypoxia</li></ul>
Describe the pathophysiology of hypoxic-ischaemic encephalopathy
<ul><li>Primary: immediately after event-> anaerobic respiration, lactic acidosis and cytotoxic oedema</li><li>Latent phase: brain appears to recover</li><li>Secondary: hours to days later-> renewed accumulation of toxic metabolites and free radicals causing further neuronal death</li></ul>
How does hypoxic-ischaemic encephalopathy present clinically?
<ul><li>Altered consciousness ranging from lethary to coma</li><li>Seizures</li><li>Abnormal tone and reflexes</li></ul>
How is hypoxic-ischaemic encephalopathy managed?
<ul><li>Supportive: maintain normal body temp and blood glucose levels</li><li>Seizure control</li><li>Neonates within 6 hours of birth: therapeutic hypothermia</li></ul>
What investigations might be done in hypoxic-ischaemic encephalopathy?
<ul><li>ABG</li><li>CBC</li><li>Electrolytes and glucose</li><li>LFTs aand U&Es</li><li>Neuoimaging: MRI and cranial USS(neonates)</li><li>EEG monitoring</li><li>Metabolic screening if atypical</li></ul>
<div><br></br></div>
<div>Diagnosis: clinical mostly</div>
Name some complications of hypoxic-ischaemic encephalopathy
<ul><li>Cerebral palsy</li><li>Seizure disorders</li><li>Cognitive impairment</li><li>Motor deficits</li><li>Sensory impairments</li><li>Microcephaly</li><li>Behavioural disorders</li><li>Multisystem organ failure of severe: CVR, renal, hepatic, resp</li></ul>
What is placenta accreta?
<ul><li>Spectrum of abnormalities of placental implantation into the myometrium of the uterine wall due to a defective decidua basalis</li></ul>
<div><img></img><br></br></div>
Name some risk factors for placenta accreta
<ul><li>Previous C section</li><li>Placenta praevia</li><li>Previous termination of pregnancy</li><li>Dilatation and curettage</li><li>Advanced maternal age</li><li>Uterine struuctural defects</li></ul>
What are the different types of placenta accreta?
<ol><li>Placenta accreta</li><li>Placenta increta</li><li>Placenta percreta</li></ol>
What is the placenta accreta type of placenta accreta?
<ul><li>Chorionic villi attach into myometrium rather than being restricted within the decidua basalis(does not penetrate through the thickness of the muscle)</li><li><img></img><br></br></li></ul>
What is placenta increta?
<ul><li>Chorionic villi invade into but not through the myometrium</li></ul>
<div><img></img><br></br></div>
What is placenta percreta?
<ul><li>Chorionic villi invade through the perimetrium(through full thickness of myometrium to the serosa)</li><li>Increased risk of uterine rupture and in severe cases may attach to other abdominal organs like the bladder/rectum</li></ul>
<div><img></img><br></br></div>
How is placental accreta diagnosed?
<ul><li>Doppler US</li><li>MRI</li><li>Can be difficult to diagnose antenatally</li></ul>
Name some complications of placenta accreta
<ul><li>Increased risk of severe postpartum bleeding</li><li>Preterm delivery</li><li>Uterine rupture</li></ul>
How is placenta accreta managed?
<ul><li>Elective C-section and hysterectomy</li><li>If fertility key: attempt placental resection</li></ul>
What are Capgras delusions?
<ul><li>Misidentification syndrome characterised by belief that the closse person is replaced by an imposter who looks physically the same</li></ul>
What is a brain abscess?
<ul><li>Collection of pus within the brain parenchyma linkes with significant morbidity and mortality</li></ul>
Name some risk factors for developing a brain abscess
<ul><li>Immunocompromised states</li><li>Congenital heart defects and endocarditis</li><li>Chronic otitis/sinusitis</li><li>IVDU</li><li>Dental head and neck procedures</li></ul>
Describe the pathogenesis of a brain abscess
4 stages:<br></br><ul><li>Early/initial cerebritis: 1-3 days</li><li>Late cerebritis: 4-9 days</li><li>Early capsule formation: 10-13 days</li><li>Late capsule formation: 14 days onwards</li></ul>
Describe the signs and symptoms of a brain abscesss
<ul><li>Headache</li><li>Focal neurological deficits</li><li>Infeciton signs: fever, n+v, meningism</li><li>Raised ICP: headache, 3rd nerve palsy, papilloedema, seizures</li></ul>
Name some differentials for a brain abscess
<ul><li>Space occupying lesions-cancer, vascular</li><li>CNS infections</li><li>Stroke</li></ul>
How is a brain abscess diagnosed?
<ul><li>MRI with gadolinium contrast-> better at detecting early cerebritis</li><li>CT for complications like hydrocephalus</li><li>Stereotactic needle aspiration</li><li>LP CONTRAINDICATED</li></ul>
Describe the management of a brain abscess
<ul><li>A-E and consider sepsis 6</li><li>Surgery: craniotomy-aspiration/excision</li><li>IV abx: 3rd gen: cephalosporing + meetronidazole</li><li>Sx management: dexamethasone for raised ICP </li></ul>
Name some complications of a brain abscess
<ul><li>Seizures</li><li>Meningitis</li><li>Ventriculitis</li><li>Hydrocephalus</li><li>Cerebral oedema</li><li>Herniation</li><li>Death</li><li>Permanent neuro deficits</li></ul>
Name some causes of space occupying lesions
<ul><li>Neoplasia: metastatic and primary CNS tumours</li><li>Vasulcar: avms/aneurysms</li><li>Infective: abscesses, TB etc</li><li>Granulomatouus disease: neurosarcoidosis</li></ul>
What is Cushing’s reflex?
<ul><li>Hypertension</li><li>Bradycardia</li><li>Irregular respirations</li></ul>
<div>Sign of raised ICP</div>
What investigations might be used for brain metastases
<ul><li>CT head-1st line in acute settings e.g. if presenting with seizures</li><li>MRI brain for details</li><li>PET scan</li><li>Biopsy</li></ul>
How are brain metastases treated?
<ul><li>Often not treatable with surgrical intervention</li><li>Chemo/radiation may be used</li><li>If metastases, often indicates stage 4 disease-> palliative care</li><li>Manage raised ICP-steroids, osmotic agents</li></ul>
What is a glioblastoma multiforme?
<ul><li>Mc primary brain tumour in adults</li><li>Malignant and highly aggressive</li><li>Associated with a poor prognosis-1 yr</li></ul>
How does a glioblastoma multiforme appear on imaging?
<ul><li>Solid tumours with central necrosis and a rim that enhances with contrast</li><li>Disruption of blood brain barrier and vasogenic oedema</li></ul>
How is a glioblastoma multiforme treated?
<ul><li>Surgical with postoperative chemo and/or radiotherapy</li><li>Dexamethasone for oedema</li></ul>
Describe the features of a meningioma
<ul><li>2nd mc primary brain tumour in adults</li><li>Typically benign, extrinsic tumours of the CNS</li><li>Aris from dura mater of the meninges and cause sx by compression noot invasion</li></ul>
How is a meningioma diagnosed and treated?
<ul><li>CT-contrast enhancement and MRI</li><li>Observation, radiotherapy or surgical resection</li></ul>
What is a vestibular schwannoma?
<ul><li>Previously acoustic neuroma</li><li>Benign tumour arising from the 8th cranial nerve</li><li>Often seen in cerebellopontine angle</li></ul>
What might be seen on histology of a vestibular schwannoma?
<ul><li>Antoni A or B patterns seen</li><li>Verocay bodies(acellular areas surrounded by nucelar palisades)</li></ul>
What is a pilocytic astrocytoma?
<ul><li>Mc primary brain tumour in children</li></ul>
What is a medulloblastoma?
<ul><li>Aggressive paediatric brain tumour that arises withn the infratentorial compartment</li><li>Spreads through CSF system</li></ul>
What is an oligodendroma?
<ul><li>Benign slow growing tumour common in the frontal llobes</li></ul>
What might be seen on histology of a patient with an oligodendroma?
<ul><li>Calcifications with a 'fried egg' appearrance</li></ul>
What is a haemangioblastoma and what is it associated with?
<ul><li>Vascular tumour of the cerebellum</li><li>Associated with von Hippel-Lindau syndrome</li></ul>
What is a pituitary adenoma?
<ul><li>Benign tumours of the pituitary gland</li><li>Either secretory or non-secreotry</li><li>Can be microadenomas(<1cm) or macroadenomas(>1cm)</li></ul>
How do patients with pituitary adenomas present?
<ul><li>Consequences of hormone excess</li><li>Cushing's: ACTH</li><li>Acromegaly: GH</li><li>Compression of optic chiasm: bitemporal hemianopia due ot crossing nasal fibres</li></ul>
How is a pituitary adenoma diagnosed?
<ul><li>Pituitary blood profile</li><li>MRI</li></ul>
How can pituitary adenomas be treated?
<ul><li>Hormonal</li><li>Surgical: transphenoidal resection</li></ul>
What is a craniopharyngioma?
<ul><li>Most common paediatric supratentorial tumour</li><li>Solid/cystic tumour of the cellar region derived from the remnants of Rathke's pugh</li><li>Can be in adults too</li></ul>
How might patients with craniopharyngioma present?
<ul><li>Hormonal distrubance</li><li>Hydrocephalus</li><li>Bitemporal hemianopia</li></ul>
What might be seen on histology of a patient with craniopharyngioma?
<ul><li>Derived from remnants of Rathke's pouch</li></ul>
How is a craniopharyngioma diagnosed?
<ul><li>Pituitary blood profile</li><li>MRI</li></ul>
How is a craniopharyngioma treated?
<ul><li>Typically surgical +/- postoperative radiotherapy</li></ul>
What is herpes zoster ophthalmicus?
<ul><li>Serious, vision threatening infection caused byt the reactivation of the varicella zoster virus within the ophthalmic division of the trigeminal nerve</li></ul>
Describe the epidemiology of herpes zoster ophthalmicus
<ul><li>Primarily older adults: 60-70yrs</li><li>Immunocompromised</li></ul>
Name some risk factors for herpes zoster ophthalmicus
<ul><li>Age: >60yrs</li><li>Immunosuppression</li><li>Past hx of chickenpox</li></ul>
Describe the presentation of a patient with herpes zoster ophthalmicus
<ul><li>Painful red eye</li><li>Fevere</li><li>Malaise</li><li>headache</li><li>Erythematous vesicular rash over the trigeminal division of the opthalmic nerve</li></ul>
<div>Hutchinson's sign: skin lesion on tip/side o fnose indicative of nasocilliary nerve involvement-> higher risk of ocular involvement</div>
Name some differentials for herpes zoster ophthalmicus
<ul><li>Bacterial conjunctivitis</li><li>Uveitis</li><li>Keratitis</li></ul>
What investigations are used to diagnose<b> </b>herpes zoster ophthalmicus
<ul><li>Ophthalmic exam to assess extent of ocular involvement and potnetial complications</li><li>Viral culture/PCR testing from skin lesions/ocular speciemens to confirm dx</li></ul>
How is herpes zoster ophthalmicus mnaged?
<ul><li>Ig Hutchinson's sign: urgen ophthalmology review</li><li>Oral aciclovir</li><li>Topical steroids-> may be used under guidance of ophthalmology to reduce inflammation and prevent scarring(caution as might exacerbate infection)</li></ul>
What is shingles?
<ul><li>Reactivation of the varicella zoster virus which can lie dormant in the nerve ganglia following primary infection(chickenpox)</li></ul>
In what age groups does shingles commonly occur?
<ul><li>Elderly</li><li>If in young person should prompt investigation for underlying immune condition</li></ul>
Describe the presentation of shingles
<ul><li>Tingling feeling in a dermatomal distribution</li><li>Progressess to erythematous papules occuring along one or more dermatomes within a few days-> develop into fluid filled vesicles which then crust over and heal</li><li>Associated with viral sx: fever, headache, malaise</li><li>Herpes zoster ophthalmicus</li></ul>
Describe the management of shingles
<ul><li>Oral antiviral(valaciclovir) within 72hr rash onset if immunocompromised or moderate/severe rash/pain or non-truncal involvemets</li><li>Hospital and IV antivirals if severe, immunocompromised/ophthalmic sx, suspicion of meningitis/encephalitis</li><li>Avoid contact with pregnany women, babies and immunocompromised until lesions are fully crusted over</li><li>Pain management with NSAIDs, back up amitryptyline, duloxetine, gabapentin</li></ul>
Name some complications of shingles
<ul><li>Secondary bacterial infection of skin lesions</li><li>Corneal ulcers, scarring and blindness if eye involved</li><li>Post herpetic neuralgia</li></ul>
Describe the features of post herpetic neuralgia
<ul><li>Pain occuring at site of healed shingles infection</li><li>Can cause neuropathic pain(burning, pins and needles)</li><li>Can cause allodynia(perception of pain from a normally non-painful stimulus like light touch)</li></ul>
Name some risk factors for normal pressure hydrocephalus
<ul><li>SAH</li><li>Meningitis</li><li>Traumatic brain injury</li><li>Intracranial tumours</li><li>Ventricular shunting or LP</li></ul>
Describe the pathophysiology of normal pressure hydrocephalus
<ul><li>Ventricular dilation without an apparent increase in intracranial pressure-> periventricular stress-> disruption of blood brain barrier-> inflammatory response-> cerebral perfusion changes</li></ul>
Name some differentials for normal pressure hydropcephalus
<ul><li>Alzheimer's</li><li>Parkinson's</li><li>Other dementias</li></ul>
How is normal pressure hydrocephalus investigated?
<ul><li>CT.MR imaging: dilated lateral ventricles-can also be seen in demenita</li><li>LP: measure walking ability and cognition before and after</li></ul>
Describe the management of normal pressure hydrocephalus
<ul><li>Therapeutic LP</li><li>Ventriculoperitoneal shunt-redirect excess CSF to abdomen</li></ul>
What is idiopathic intracranial hypertension?
<ul><li>AKA psudotumour cerebri/benign intracranial hypertension</li><li>Increased intracranial pressure without any clear cause evident on neuroimaging and other investigations</li></ul>
Describe the epidemiology of idiopathic intracranial hypertension
<ul><li>Young and obese women</li><li>9:1 women</li></ul>
Name some risk factors for idiopathic intracranial hypertension
<ul><li>Femal gender</li><li>Obesity</li><li>Pregnancy</li></ul>
Name some differentials for idiopathic intracranial hypertension
<ul><li>Brain tumour</li><li>Venous sinus thrombosis</li><li>Sleep apnoea</li><li>Migraines</li></ul>
What investigations might be done in a patient with suspected idiopathic intracranial hypertension
<ul><li>Ophthalmoscopy-> bilateral papilloedema</li><li>CT/MRI: increased ICP, MRI venogram to rulee out venous sinus thrombosis</li><li>LP: KEY: opening pressure >20cmH20. Rule out other causes: CSF profile should be normal</li></ul>
Describe the management of idiopathic intracranial hypertension
<ul><li>Weight losss</li><li>Carbonic anhydrase inhibitors-acetazolamide-poorly tolerated</li><li>Topirimate and candesartan</li><li>Invasive: therapeutic LP, surgical CSF shunting, optic nerve sheath fenestration-prevent progressive visual loss</li></ul>
Describe the prognosis of idiopathic intracranial hypertension
<ul><li>Most patients have benign course-smal proportion develop severe vissual impairment or blindness</li></ul>
<div>Visual morbidity: mostly mainly from delay in diagnosis or inadequate treatment</div>
<div>Even modest weight loss can significantly reduce pressure</div>
What is narcolespy?
<ul><li>Neurological condiiton that distrubs the sleep wake cycles</li><li>Excessive sleepiness during daytime and may also suddnely fall asleep during activities-early onset of REM sleep</li></ul>
What gene is narcolepsy associated with?
<ul><li>HLA-DR2</li></ul>
What is narcolepsy associated with low levels of?
<ul><li>Orexin(hypocretin)-> protein responsible for controlling appetitie and sleep patterns</li></ul>
How is narcolepsy investigated/diagnosed?
<ul><li>Multiple sleep latency EEG</li></ul>
Describe the management of narcolepsy
<ul><li>Daytime stimulants(e.g. modafanil)</li><li>Nighttime sodium oxybate</li></ul>
What is motor neurone disease?
<ul><li>Group of progressive neurological disorders that destroy motor neurones: the cells that control voluntary muscle activity</li></ul>
Describe the epidemiology of motor neurone disease
<ul><li>M>F</li><li>50-60yrs</li><li>90% sporadic, 10% familial</li></ul>
Name some genes associated with familial MND
<ul><li>SOD1</li><li>FUS</li><li>C9ORF72</li></ul>
What condition overlaps with MND?
<ul><li>Fontotemporal dementia</li><li>C90RF72 mutation found in both</li></ul>
Name some UMN signs
<ul><li>Spasticity</li><li>Hyperreflexia</li><li>Upgoing plantars(alhtouth often downgoing n MND)</li></ul>
Name some LMN signs
<ul><li>Fasciculations</li><li>Muscle atrophy</li></ul>
Describe the general presentation of a patient with MND
<ul><li>Combination of lower and upper MN signs</li><li>Fasciculations</li><li>Asymmetric limb weakness</li><li>Wastig of small hands muscles</li><li>Absence of sensory signs/sx</li></ul>
What are the different types of MND?
<ul><li>Amyotrophic lateral sclerosis(ALS)-most common</li><li>Primary lateral sclerosis</li><li>Progressive muscular atrophy</li><li>Progressive bulbar palsy</li><li>Spinal muscular atrophy</li></ul>
Describe the features of amyotrophic lateral sclerosis(ALS)
<ul><li>Typically LMN signs in arms and UMN in legs</li><li>If familial: gene is on chromosome 21 and codes for superoxide dismutase</li><li>Can have bulbar onset in some cases</li></ul>
Describe the features of primary lateral sclerosis
<ul><li>UMN signs only</li></ul>
Describe the features of progressive musclular atrophy
<ul><li>LMN signs only</li><li>Distal muscles before proximal</li><li>Best prognosis</li></ul>
Describe the features of progressive bulbar palsy
<ul><li>UMN and LMN signs</li><li>Palsy of tongue, muscle of masticaiton and facial muscles due to loss of function of brainstem motor nuclei-> dysphagia/dysarthria</li><li>Carries worst prognosis</li></ul>
Name some differentials for MND
<ul><li>MS</li><li>Chronic inflammatory demyelinating neuropathy</li><li>Myasthenia gravis</li><li>Brainstem lesions</li><li>Paraproteinaemias</li></ul>
How is MND investigated/diagnosed?
<ul><li>Clinical</li><li>Nerve conduction studies-> normal motor conduction so exclude a neuropathy</li><li>EMG: reduced number of action potentials with increased amplitude</li><li>MIR: brasintem lesions/cervical cord compression/myelopathy</li></ul>
Describe the management of MND
<ul><li>Mostly supportive </li><li>Riluzole-> extends life expectancy by about 3 months, used mainly in ALS</li><li>Respiratory care: BIPAP at night</li><li>Nutrition: PEG as bulbar disease progresses</li><li>Discuss advanced care early</li><li>Anticholinergics for drooling</li></ul>
How does riluzole work?
<ul><li>Prevents stimulation of glutamate receptors</li></ul>
Describe the prognosis of MND
<ul><li>Poor: 50% die within 3 years</li><li>Most <5yrs</li><li>Most die from respiratory complications</li></ul>
What is myopathy?
<ul><li>Condition affecting skeletal muscles</li></ul>
Describe the features of myopathy
<ul><li>Symmetrical muscle weakness(proximal > distal)</li><li>Problems rising from chair/getting out of bath</li><li>Normal sensation, normal reflexes, no fasciculation</li></ul>
Name some causes of myopathy
<ul><li>Inflammatory: polymyositis</li><li>Inherited: Duchenne/Becker muscular dystrophy, myotonic dystrophy</li><li>Endocrine: Cushing's, thyrotoxicosis</li><li>Alcohol</li></ul>
What is degenerative cervical myelopathy?
<ul><li>Spinal cord dysfunction from compression in the neck</li></ul>
Name some risk factors for degenerative cervical myelopathy
<ul><li>Smoking</li><li>Genetics</li><li>Occupation-> high axial loading</li></ul>
Describe the presentation of a patient with degenerative cervical myelopathy
<ul><li>Variable-fluctuating but progressive</li><li>Pain-neck, upper, lower limbs</li><li>Loss of motor function-hard to do up shirts/use a fork</li><li>Loss of sensory function-> numbness</li><li>Loss of autonomic function-> urinary/faecal incontinence and impotence</li><li>Hoffman's sign</li></ul>
What is Hoffman’s sign?
<ul><li>Used for cervical myelopathy<br></br></li><li>Flick one finger on a patients hand-> positive if reflex twitching of other fingers on same hand</li></ul>
How is degenerative cervical myelopathy diagnosed?
<ul><li>MRI cervical spine: disc degeneration and ligament hypertrophy with accompanying cord signal change</li></ul>
What is degenerative cervical myelopathy sometimes misdiagnosed as?
<ul><li>Carpal tunnel</li></ul>
Describe the management of degenerative cervical myelopathy
<ul><li>Urgent assessment by specialist spinal services-> early treatment to prevent rpogression</li><li>Surgical decompression</li><li>Physio-only by specilaist services to avoid further damage</li></ul>
What conditions affect the dorsal column?
<ul><li>Tabes dorsalis(neurosyphilis)</li><li>Subacute combined degeneration of spinal cord</li></ul>
What is the anal sphincter innervated by?
<ul><li>S2,3,4</li></ul>
What is a spinal cord compression and how is it different to cauda equina?
<ul><li>Form of myelopathy caused by pressure on cord-> causes an UMN lesion</li><li>Cauda equina: compression below level of L1-> LMN</li></ul>
Name some causes of spinal cord compression
<ul><li>Trauma: mc-vertebral fracturas/dislocation of facet joints</li><li>Malignancy</li><li>Infection: TB and abscess formation</li><li>Epidural haematoma</li><li>Intervertebral disco prolapse-rare</li></ul>
Describe the symptoms of a patient with spinal cord compression
<ul><li>Back pain: severe, progressive and aggravated by straining(couhging etc)</li><li>Difficulty walking</li><li>Weakness/numbess bleow level compressed(usually bilateral and symmetrical)</li><li>Incontinence</li><li>Urinary retention</li><li>Constipation</li><li>Systemi e.g. weight loss, fatigue, fevers if MSCC/TB</li></ul>
Name some signs seen in a patient with spinal cord compression
<ul><li>Hypertonia</li><li>Hyperreflexia(may be absent at level compressed)</li><li>Clonus</li><li>Upgoing plantars</li><li>Sensory loss</li></ul>
Name some differentials for spinal cord compression
<ul><li>Transverse myelitis</li><li>Cauda equine</li><li>Peripheral neuropathy</li><li>Spinal metastases</li><li>Sciatica</li></ul>
How is spinal cord compression investigated/diagnosed?
<ul><li>MRI whole spine-urgent if suspected MSCC</li><li>Bladder scan if suspected urinary retention</li><li>EEG and baseline bloods</li><li>If MSCC: ix to find primary cancer</li></ul>
Describe the management of spinal cord compression
<ul><li>Immobilise and spinal precautions</li><li>Analgesia for pain</li><li>VTE prophylaxis</li><li>Catheteris if retention</li><li>Treat underlying cause</li><li>Neurosurgery-> consider surgical decompression</li></ul>
Describe the management of metastatic spinal cord compression
<ul><li>Hihg dose steroids: 16mg dexamethasone to reduce oedema and compression +PPI + monitor glucose</li><li>Refer to neuro: surgical decompression(vertebroplasty/kyphoplasty)</li><li>Oncology input</li></ul>
In patients with metastatic spinal cord compression where do the metastases most commonly come from?
<ul><li>Lung</li><li>Breast</li><li>Prostate</li></ul>
What is cauda equina syndrome?
<ul><li>Lumbosacral nerve roots that extend below the spinal cord(L1/L2 level) are compressed</li></ul>
Name some causes of cauda equina syndrome
<ul><li>Lumbar disc herniation at L4/5 or L5/S1-mc</li><li>Tumours-primary/metastatic</li><li>Trauma</li><li>Infection: abscess, discitis</li><li>Epidural haematoma</li></ul>
Describe the symptoms of cauda equina syndrome
<ul><li>Low back pain</li><li>Radicular pain-often symmetrical</li><li>Leg weakness</li><li>Difficulty walking</li><li>Saddle anaesthesia</li><li>Bowel incontinence/constipation</li><li>Urinary incontience/retention</li><li>Erectile dysfunction or sexual dysfunction</li></ul>
Describe the signs of cauda equina syndrome
<ul><li>Loss of lower limb power</li><li>Hypotonia in lower limbs</li><li>Hyporeflexia in lower limbs</li><li>Sensory loss/paraesthesias in legs</li><li>Reduced perianal sensation</li><li>Loss of anal tone</li><li>Bladder palpable and dull to percussion in urinary retention</li></ul>
Name some differentials for cauda equina syndrome
<ul><li>Compression of ocnus medullaris</li><li>Spinal cord compression</li><li>Sciatica</li></ul>
How is cauda equina syndrome diagnosed?
<ul><li>Urgent whole spine MRI</li></ul>
Describe the management of cauda equina syndrome
<ul><li>Surgical decompression</li></ul>
Name some complications of cauda equina syndrome
<ul><li>Permanent paralysis of lower limbs</li><li>Sensory loss</li><li>Bladder/bowel dysfunction</li><li>Sexual dysfunction</li><li>Pressure ulcers</li><li>VTE due to immobility</li></ul>
If damage to the DCML occurs in the spinal cord, what side will the symptoms be?
<ul><li>Same side</li></ul>
What is sub-acute combined degeneration of the spinal cord?
<ul><li>Degeneration of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts associated with vitamin B12 deficiency</li></ul>
Describe the signs and symptoms of a patient with sub-acute combined degeneration of the spinal cord
<ul><li>Symmetrical distal sensory sx, usually start at feet and progress to hands</li><li>Varying degrees of ataxia</li><li>Mixed UMN and LMN sings: exaggerated/diminished/absent reflexes</li><li>Autonomic bowel/bladder sx</li><li>Haematological manifestations may be present/absent</li></ul>
How is sub-acute combined degeneration of the spinal cord investigated/diagnosed?
<ul><li>Assess B12 and folate</li><li>Homocysteine: raised level despite normal B12-> functional B12 deficiency</li><li>MRI of spine-exclude myelopathy</li><li>Nreve conduction studies: axonal neuropathy</li></ul>
Describe the management of sub-acute combined degeneration of the spinal cord
<ul><li>Urgent Vitamin B12 repkacement using hydroxocobalamin 1mg IM alternate days until no further imporvement</li><li>Maintainence tx with hydroxocobalamin 1g IM every 2 months</li></ul>
What are muscular dystrophies?
<ul><li>Group of inherited genetic disorders characterised by progressive degeneration and weakening of muscles</li></ul>
Name some types of muscular dystrophies
<ul><li>Duchenne Muscular Dysrophy</li><li>Becker muscular dystrophy</li></ul>
Describe the symptoms of Duchenne muscular dystrophy
<ul><li>Progressive proximal muscle weakness from 5 years</li><li>Calf pseudohypertrophy</li><li>intellectual impariment</li><li>Gower's sing: child uses arms to stand from a squatted position</li></ul>
Describe the features of Becker’s muscular dystrophy
<ul><li>Presents later in childhood with muscle wasting and weakness</li><li>Wheelchair bound in teens and can survive into thirties</li></ul>
How is Duchenne muscular dystrophy investigated/diagnosed?
<ul><li>Raised creatinine kinase</li><li>Genetics-replaced muscle biopsy</li></ul>
Describe the management of Duchenne muscular dystrophy
<ul><li>Supportive: low impact exercise, mobility aids, OT, physio</li><li>Manage complications: dysphagia, chest infections etc</li><li>Glucocorticoids: slow muscle regeneration for 6 months-2 years</li><li>Newer: ataluren and creatinine supplemebts</li><li>Genetic counselling</li></ul>
What is the prognosis like for Duchenne and Becker’s muscular dystrophy
<ul><li>Most children can't walk by age 12</li><li>Typicaly survive to age 25-30yrs</li><li>Better for Becker's: live into 30s</li></ul>
Name some complications of Duchenne muscular dystrophy
<ul><li>Joint contractures</li><li>Respiratory muscle failure-hypoventilation, poor cough and recurrent pneumonia(cause of death)</li><li>Dilated cardiomyopathy</li><li>Anaesthetic complications(rhabdo and malignant hyperthermia</li></ul>
Describe the epidemiology of migraine
<ul><li>Common</li><li>F>M</li><li>Peak: 30-39yrs</li></ul>
Name some triggering factors for migraines
<ul><li>Tiredness/stress</li><li>Alcohol</li><li>COCP</li><li>Lack of food/hydraiton</li><li>Cheese, chocolate, red wines, citrus fruits</li><li>Menstruation</li><li>Bright lights</li></ul>
How might migraines present in children?
<ul><li>May be shorter lasting</li><li>Bilateral headaches</li><li>More prominent GI disturbance</li></ul>
Describe the symptoms of a migraine
<ul><li>Aura: visual/sensory sx preceding headache</li><li>Unilateral throbbing headache</li><li>Photophobia/phonophobia</li><li>Nause ande/or vomiting</li></ul>
Name some differentials for a migraine
<ul><li>Tension type headache</li><li>Cluster headache</li><li>SAH/stroke</li><li>Giant cell arteritis</li></ul>
Describe the features of a hemiplegic migraine
<ul><li>Migraine variant in which motor weakness is a manifestation of aura in at least some attacks</li><li>Strong family history in 50%</li><li>Very rare, most common in adolescent females</li></ul>
What aura symptoms of a migraine might prompt further investigation/referral?
<ul><li>Motor weakness</li><li>Double vision</li><li>Visual sx in only one eye</li><li>Poor balance</li><li>Decreased level of consciousness</li></ul>
Describe the prophylactic management of migraines
<ul><li>Propanolol-CI in asthma</li><li>Topirimate-not for women of childbearing age/onc ontraceptive</li><li>Amitryptaline</li><li>Candesartan</li></ul>
<div><br></br></div>
<div>Injections:</div>
<div><ul><li>Greater occipital nerve block</li><li>Botulinum toxin injections</li><li>Acupuncture </li></ul></div>
Describe the general management if migraines with regards to drug classes
<ul><li>5 HT receptor agonists for acute</li><li>5 HT receptor antagonists for prophylaxis</li></ul>
What is the problem with regular use of acute migrain medications?
<ol><li>If used >10-15 days/month-> medication overuse headache</li></ol>
Describe the treatment of migraines in pregnancy
<ul><li>Paracetemol 1g first line</li><li>NSAIDS second line in 1st and 2nd trimester</li><li>Avoid aspirin and opioids like codeine</li></ul>
How does a PMH of migraines affect COCP and HRT use?
<ul><li>COCP: absolute contraindication in patients with aura due to risk of stroke</li><li>HRT: safe to prescribe but may make migraines worse</li></ul>
Name some red flags for headaches
<ul><li><20yrs+ hx of cancer</li><li>Vomiting wihtout other obvious cause</li><li>Worsenign headache iwth fever</li><li>Thunderclap headache</li><li>New onset neuro deficit/cognitive dysfunction/consciousness/personality changes</li><li>Recent head trauma</li><li>Headache triggered by cough, sneeze or exercise or orthostatic headache</li><li>Sx suggestive of GCA or acute narrow angle gluacoma</li></ul>
Name some risk factors for cluster headaches
<ul><li>Male</li><li>>30yrs</li><li>Alcohol consumption</li><li>Prior brain surgery/trauma</li><li>Fhx</li></ul>
How are cluster headaches diagnosed/investigated?
<ul><li>Generally clinical diagnosis but neuroimaging done in most patients-underlying brain lesion can be found in some patients</li><li>MRI with gadolinium contrast</li></ul>
Describe the prophylactic treatment for cluster headaches
<ul><li>Verapamil</li><li>Topirimate</li><li>Sometimes tapering dose of prednisolone</li></ul>
What is needed to be monitored if treating a patient with verapamil?
<ul><li>ECG to check cardiac function</li></ul>
Describe the epidemiology of tension headaches
<ul><li>Mc cause of chronic recurring head pain</li><li>Women?men</li></ul>
Name some contributing factors to tension headaches
<ul><li>Stress</li><li>Poor posture</li><li>Eye strain</li></ul>
How is a tension headache managed?
<ul><li>Stress management</li><li>PT</li><li>Analgeisa: paracetemol or NSAIDS then step it up</li><li>Be careful of mediaction overuse headaches</li></ul>
What is a central venous sinus thrombosis?
<ul><li>Occlusion of venous vessels in sinuses of the cerebral veins</li></ul>
Name some risk factors for central venous sinus thrombosis
<ul><li>Hormoanl(pill, pregnancy etc)</li><li>Prothrombotic haem conditions/malignancy</li><li>Systemic disease(dehydration/sepsis)</li><li>Local(skull abnormaliites, trauma, local infection</li></ul>
Describe the presentation of central venous sinus thrombosis
<ul><li>Very variable</li><li>Headache</li><li>Confusion/drowsiness/impaired consciousness</li><li>IMpaired vision</li><li>N+V</li><li>Focal neuro deficits</li><li>Cranial nerve palsies</li><li>Papilloedema</li><li><br></br></li></ul>
How is central venous sinus thrombosis investigated/diagnosed?
<ul><li>NCCT head: hyperdenstiy in affected sinus</li><li>CT venogram-filling defect-empty delta sign</li></ul>
What is the most common form of dural venous sinus thrombosis
<ul><li>Superior sagittal sinus</li></ul>
How is central venous sinus thrombosis treated?
<ul><li>LMWH</li><li>Adress undelying risk factors that increase risk of clotting</li><li>After initial therapy with LMWH can be bridged to warfarin</li></ul>
How do patients with central venous sinus thrombosis present?
<ul><li>Chemosis</li><li>Exophthalmos</li><li>Peri-orbital swelling</li></ul>
What is Brown-Sequard syndrome?
<ul><li>Lateral hemisection of the spinal cord</li></ul>
<div><img></img><br></br></div>
Name some causes of Brown-Sequard syndrome
<ul><li>Cord trauma-penetratin injury mc</li><li>Neoplasms</li><li>Disc herniation</li><li>Demyelination</li><li>Infective/inflammatory lesions</li><li>Epidural haematomas</li></ul>
Describe the management of Brown-Sequard syndrome
<ul><li>Depends on causative pathology</li><li>Medical management preferred if infective/inflammatory/demyelinating</li><li>Surgical if pathologies causing extrinsice cord compression</li></ul>
What is the spinothalamic tract responsible for?
<ul><li>Anterolateral cord</li><li>Contralateral pain and temperature sensation</li></ul>
What is the dorsal column tract responsible for?
<ul><li>Posterior cord</li><li>Ipsilateral vibration and proprioception</li></ul>
What is the lateral corticospinal tract responsible for?
<ul><li>Ipsilateral movement of limbs</li></ul>
What is mononeuropathy?
<ul><li>Damage/dysfunction of a single peripheral nerve-> most cause motor and sensory impairment</li></ul>
What is the most common mononeuropathy?
<ul><li>Carpal tunnel syndrome</li></ul>
What are the general symptoms of mononeuropathies
Depends on underlying cause and affected nerve<br></br><ul><li>Sensory: numbness, pain, tingling</li><li>Motor: weakness, atrophy, loss of coordination</li></ul>
How are mononeuropathies generally treated?
<ul><li>Conservative: rest, heat, avoid/remove causative activity, NSAIDs, bracing</li><li>Oral/injected corticosteroids</li><li>Surgical decompression</li></ul>
What is carpal tunnel syndrome?
<ul><li>Compression of median nerve in the carpal tunnel</li></ul>
<div><img></img><br></br></div>
In what circumstances is carpal tunnel commonly seen in?
<ul><li>Repetitive wrist activites</li><li>Systemic disease: diabetes/RA</li><li>Pregnancy</li><li>Anatomical variations</li></ul>
<div>Anything that causes an increase in pressure within the carpal tunnel or decreases the tunnel's size</div>
Describe the symptoms of carpal tunnel syndrome
<ul><li>Pain and paraesthesia in thumb index and middle finger-impingement of palmar digital branch of median nerve</li><li>Symptoms worse at night or after activities involving writs flexion</li></ul>
What might be seen on examination in a patient with carpal tunnel syndrome?
<ul><li>Weakness of thumb abduciton(abductor pollicis brevis)</li><li>Wasting of thenar eminence NOT hypothenar</li><li>Tinel's signL tapping causes paraesthesia</li><li>Phalen's sign: felxion of wrist causes sx</li></ul>
Name some differentials for carpal tunnel syndrome
<ul><li>Cubital tunnel syndrome</li><li>Thoracic outlet syndrome</li><li>Radial tunnel syndrome</li><li>Ulnar neuropathy</li></ul>
How is carpal tunnel diagnosed?
<ul><li>EMG and nerve conducton studies: motor+sensory prolongation of action potential</li></ul>
Describe the management of carpal tunnel syndrome
<ul><li>Conservative: splints at night, NSAIDS, corticosteroid injecitons, adjust activities </li><li>Surgeryical decompression: flexor retinaculum division</li></ul>
What is radiculopathy?
<ul><li>Symptoms cuased by compression off a nerve root in the spinal common</li></ul>
<div><img></img><br></br></div>
How can radiculopathy be classified?
<ul><li>Cervical</li><li>Lumbar</li></ul>
Describe the sympotms of cervical radiculopathy
<ul><li>Pian in neck, shoulders, upper back or arms</li></ul>
What age group is most commonly affected by cervical radiculopathy
<ul><li>30-60yrs</li></ul>
Name some causes of cervical radiculopathy
<ul><li>Disc degeneration</li><li>Sponylosis</li><li>Bone disease</li><li>Cancer</li><li>Herniated disc</li></ul>
Name 2 examples of lumbar radiculopathy
<ul><li>Sciatica-mc</li><li>Cauda equina syndrome</li></ul>
Describe the symptoms of sciatica
<ul><li>Pain and numbness from spinal nerve root location to legs or feet</li></ul>
Name some causes of lumbar radiculopathy
<ul><li>Disc herniation</li><li>Bone spurs</li><li>Bone disease</li><li>Cancer</li></ul>
Describe the treatment for radiculopathy
<ul><li>OTC anaglesia</li><li>PT: lower pain, improve posture, strengthen muscles</li><li>Steroid injecitons</li><li>Oral steroids</li><li>Anti-epileptics</li><li>Surgical spinal decompression</li></ul>
