Neurology mc qs
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Neurology mc qs Neurology mc qs Presentation Transcript

  • Trickier Neurology Clinical Syndromes for the AMK By Olivia Jagger Academic Education F2
  • Examination findings and causes Upper Motor Neurone Lower Motor Neurone Tone Spastic Normal Reflexes Increased Decreased or absent Clonus ?+ve (ankles) -ve Wasting Absent (disuse wasting) Present Fasiculation Absent ?Present (esp MND) Plantars Extensor Flexor or absent Causes Stroke, MS, MND Guillain Barre, MND
  • A 34-year old woman presents to A+E with a two day history of increasing headache and confusion. She has a temperature of 38.2 degrees. Whilst in the emergency department she has a tonic-clonic seizure. MRI shows increased signal in the temporal lobes on T2 imaging. What is the most likely cause? A. Alcohol intoxication B. Severe pneumonia C. Viral encephalitis D. Subarachnoid haemorrhage E. Hepatic encephalopathy
  • • Followed by acute or subacute onset of: a notifiable disease Herpes Simplex Encephalitis Altered consciousness Focal and generalised seizures Features of raised intracranial pressure Psychiatric symptoms, behavioural abnormalities, confusion and delirium Focal neurological signs, including hemiparesis and cranial nerve lesions • Investigations MRI head - commonly affects the temporal lobes. LP. Culture of organisms is usually unsuccessful. PCR of the CSF is test of choice. Diagnosis can also be made by the
  • A 53-year-old woman has a one-week history of sudden onset of weakness of the left side of her face. On examination she has a leftsided facial droop with difficulty on the left side in raising her eyebrow, closing her eye and blowing out her cheek. What is the most likely diagnosis? A. Myasthenia gravis B. Lacunar infarct C. Multiple sclerosis D. Bell’s palsy E. Middle cerebral artery infarct
  • A 51 year old gentleman is referred by his GP for worsening back pain. He works as an electrician and is concerned that he is unable to work due to the pain. On questioning, he has had 'niggling pain' in his lower back for a few months but this morning, 4 hours prior to presentation he notes that all of a sudden the pain became far worse, very sharp in nature with no radiation. He notes that he wants to pass urine but feels unable to and is complaining of saddle anaesthesia. • Which is the most appropriate diagnosis? sciatica mechanical back pain cauda equina syndrome syringomyelia prolapsed disc
  • A 51 year old gentleman is referred by his GP for worsening back pain. He works as an electrician and is concerned that he is unable to work due to the pain. On questioning, he has had 'niggling pain' in his lower back for a few months but this morning, 4 hours prior to presentation he notes that all of a sudden the pain became far worse, very sharp in nature with no radiation. He notes that he wants to pass urine but feels unable to and is complaining of saddle anaesthesia. • Which is the most appropriate diagnosis? Thoraco-lumbar spine Xrays MRI spine Bloods including erythrocyte sedimentation rate and C-reactive protein CT head Nerve conduction studies
  • Cauda Equina - neurological emergency! Commonest cause is central disc prolapse Compression of central sacral or lumbar roots Sciatica Loss of bladder / bowel control / sexual dysfunction Saddle sensory loss Perianal sensory loss and sphincter disturbance Lower limb weakness (decreased/lost reflexes, paraesthesia) Urgent lumbar MRI and surgical referral for decompression
  • • • A 25-year-old man develops sudden weakness of the legs followed a few days later by weakness in the arms associated with ‘pins and needles’. He is normally well apart from 3 days of diarrhoea about 2 weeks before. On examination he has weakness in all four limbs and his reflexes are absent. What is the most appropriate diagnosis? Peripheral neuropathy Brainstem lesion Spinal Cord Compression Guillain-Barre syndrome Brown-Sequard syndrome
  • • • A 25-year-old man develops sudden weakness of the legs followed a few days later by weakness in the arms associated with ‘pins and needles’. He is normally well apart from 3 days of diarrhoea about 2 weeks before. On examination he has weakness in all four limbs and his reflexes are absent. What is the most appropriate investigation? Vital Capacity CSF Viral blood screen Nerve conduction tests Chest Xray
  • Guillain-Barre Syndrome Presentation Autoimmue attack v myelin antigens 60% have antecedent infection (EBV, CMV, campylobacter) Syndrome about 2 weeks later Sensory symptoms in toes (paraesthesia), followed by weakness in legs (areflexia and later wasting) Weakness ascends over 10-14 days (can involve face and respiratory muscles) can be associated with back pain
  • GBS - Investigations and Management CSF: raised protein, absence of WBCs Nerve conduction studies normal in early stages ? recent infection (viral screen) Monitor Vital Capacity (+ / - ventilation) Best nursed on HDU / ITU ECG (occ heart block) IVIg if evolving significant weakness Analgesia 5% mortality; 10% permanent disability
  • A 67-year-old woman had a 3 month history of weakness of his left leg and a 1 month history of weakness in both arms. He felt things were getting progressively worse. On examination he had wasting and fasciculations in all four arms. He was weak in all four limbs with brisk reflexes throughout with upgoing plantars. He had a normal sensory examination. What is the most likely diagnosis? • What is the most appropriate diagnosis? Parkinson’s disease Multiple sclerosis Motor neurone disease Myasthenia gravis Huntington’s Chorea
  • Motor Neurone Disease - Signs Combination of UMN and LMN signs (selective of MOTOR neurones) Wasting / weakness small muscles hands (LMN) Fasiculations upper limbs / shoulders (LMN) leg weakness / brisk reflexes / extensor plantars (spastic) (UMN) Bulbar / pseudobulbar palsy - affects speech / swallow (LMN/UMN)
  • Motor Neurone Disease Diagnosis and Management Diagnosis mainly clinical (Absence of sensory symptoms / signs, CK moderately increased, NCS show denervation) Aetiology unknown, 10% dominantly inherited Life expectancy on average 4 years Management - supportive (SALT, OT, PEG, +/- Riluzole)
  • A 25-year-old woman develops a painful visual disturbance in her left eye. She had previously had an episode of ataxia a year earlier lasting a few months. What is the most appropriate diagnosis? Parkinson’s disease Multiple sclerosis Motor neurone disease Myasthenia gravis Huntington’s Chorea
  • Multiple Sclerosis Inflammatory demyelinating CNS disorder - Disease of the white matter relapsing/remitting, secondary progressive, primary progressive Acute attack: - Optic neuritis (optic nerve) - Transverse myelitis (spinal cord) - Diplopia (brainstem) Late disease: spastic paraplegia, incontinance, dementia, cerebella ataxia, bilateral intranuclear opthalmoplegia
  • Multiple Sclerosis Investigations: Brain MRI / LP (oligoclonal banding) Acute Management: steroids Disease modifying agents: Betainterferons, Natalizumab Other treatments: PT, OT, antispasmotic agents (baclofen), ??Vit D
  • A 50-year-old woman presents with difficulty keeping her head up. She has proximal weakness in the arms which is fatigable. She comments that he speech becomes very slurred towards the end of the day and she is finding it difficult to swallow. • What is the most appropriate diagnosis? Stroke Parkinson’s disease Multiple Sclerosis Myasthenia Gravis Huntington’s disease
  • Myasthenia Gravis - presentation • Aetiology ✴Autoimmune condition. Antibodies attack the postsynaptic acetylcholine receptors at the neuromuscular junction, leading to decreased conduction at NMJ and muscle fatigue/ weakness. ✴Disease has a fluctuating pattern of ‘crises’ and remittances. ✴Very strong association with disorders of the THYMUS. In 75% of patients with Myasthenia Gravis there is hyperplasia of the thymus, and in 10% this becomes a thymoma. • Symptoms ✴Weakness in muscles, particularly the ocular, bulbar, proximal skeletal and axial. (Respiratory muscles can be involved). ✴Fatigability is a key symptom! day. Symptoms get worse at the end of the
  • •Investigations MG -tests for serum acetylcholine receptor antibodies Investigation / Treatment ✴Blood ✴Nerve conduction studies ✴CT/ MRI scans - to image the thymus ✴Vital Capacity (Spirometry / peak flow) may need respiratory support ✴Ice cube test - place over ptosis for 2mins, eye opens. Though that low temperatures improve neuromuscular transmission. • Treatment ✴Acetylcholinesterase inhibitors (neostigime) increase the amount of Acetylcholinesterase available to functioning receptors.
  • A 66-year-old man is finding that he has more difficulty getting up and moving about for the past year. He is annoyed by a tremor in his hands, but the tremor goes away when he performs routine tasks using his hands. His friends remark that he seems more sullen and doesn't smile at them, but only stares with a fixed expression on his face. He has not suffered any loss of mental ability. • Which of the following conditions is he most likely to have? Parkinson’s disease Recurrent TIA’s Huntington’s disease Myasthenia Gravis Motor Neurone Disease
  • Parkinsons - clinical features Pathology: loss of dopaminergic neurons from the substania nigra. Surviving neurons often contain Lewy bodies (collections of proteins - α-synuclein). Aetiology: most commonly idiopathic (can be drug induced and several genetic ‘parkinsons plus’ syndromes) Clinical features: TRIAD 1) resting tremor 2) rigidity 3) bradykinesia Other typical signs/symptoms: Festinating gait - stooped, shuffling, narrow based, slow to start then accelerates, with swinging arms, Hypomimia (and reduced blinking rate - glabellar tap), Hypographia, Depression, Hallucinations, Lewy body dementia, Anosmia. Power and reflexes are normal (extra-pyramidal)
  • Parkinsons - treatment Dopamine cannot cross the BBB, but its precursor L-DOPA can, and once it has, it is converted to dopamine by DOPA decarboxylase. Acts by increasing levels of free dopamine in the brain. Short half-life. Therefore, L-Dopa is given with a decarboxylase inhibitor (carbidopa, entacapone or benserazide) to prevent peripheral breakdown and prolong the half-life of L-dopa, reducing the dose needed by about 90%! • • • • • Side Effects Efficacy decreases over time ‘On-off effect’ at the end of the dose Nausea / GI Upset Dyskinesias
  • Other neuro conditions you should be familiar with ...
  • ✴ Unilateral ✴ Visual disturbance – zigzag lines Migraine - Classical Features ✴ Changes in sensation of face ✴ Vomiting/nausea/abdominal pain ✴ Aura/halo ✴ Daytime onset ✴ Relieved by sleep ✴ Have to lie in a quiet, dark room (photophobia and noise adversion) ✴ FH migraine ✴ Are they on COCP? (CI in migraines) ✴ Can have focal signs (i.e. arm/leg weakness)
  • • Meningitis a notifiable disease! Signs and Symptoms Photophobia Stiff neck Rash (non-blanching) Treatment •Start antibiotics immediately if suspecte •At GP/in ambulance - IM Benzylpenicilli •At Hospital - IV Ceftriaxone Systemically unwell Contact with meningitis • Investigations CT head prior to LP to ensure no raised intracranial pressure LP - increased protein (inflammation) and WCC (infection) and low glucose (gobbled up by bacteria). May culture an organism (commonly Neisseria meningitidis)
  • ✴ Occipital ✴ SEVERE - peak intensity within seconds Subarachnoid Haematoma ✴ Associated vomiting ✴ Occasionally seizures ✴ FH of berry aneurysms (related to Polycystic Kidneys) • Investigation ✴ CT angiogram ✴ LP (if normal CT) looking for xanthochromia broken down RBC in CSF • Treatment:
  • ✴Worse in the mornings Space-occupying lesion ✴Night time wakening ✴Worse when lying flat / coughing / bending down ✴Associated with vomiting ✴Visual changes ✴Facial nerve palsy ✴Seizures ✴Papilloedema • Tumours ✴Abnormal movements – abnormal gait/loss of coordination
  • • Bells Palsy Signs and Symptoms Rapid onset unilateral facial nerve weakness. Patient unable to show teeth, crew up eye and raise eyebrows on affected side Severe cases may also present with notable loss of taste sensation (anterior 2/3 of tongue), intolerance of high-pitched noises, mild dysarthria. Lower Motor Neuron Signs (LMN) Can be distinguished from an UMN lesion (e.g. a stroke) by testing if the forehead is affected ◦ Forehead normal – UMN lesion – due to bilateral cortical representation and innervation of the forehead ◦ Forehead affected – LMN lesion
  • Good Luck! Remember, some of the possible answers you will know and be able to exclude / rule in Think what signs the question scenario is describing UMN or LMN Some extra reading, look up Stroke and Epilepsy. Any questions to olivia.jagger@nhs.net