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166 Cards in this Set
- Front
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Symptoms of cluster headache
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Rapid onset severe pain around 1 eye which may become watery and bloodshot with lid swelling, lacrimation, facial flushing, and rhinorrhoea. Pain is unilateral, can last between 15 mins and 3 hrs, and is more common at night.
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Most common pathogens in meningitis
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N. meningitidis, S. Pneumoniae, H. Influenzae, Listeria (immunocompromised)
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Pathogens by age/risk factors in meningitis
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Babies - Group B strep, E. Coli
Older children and adults - N. meningitidis, S. Pneumoniae Elderly/immunocompromised = Listeria AIDs patient? = TB |
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Clinical clues in meningitis
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Petechial rash = meningococcal infection (do NOT do LP until clotting screen is back)
Skull fracture, ear disease, congenital CNS lesion = pneumococcal infection |
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Meningitis antibiotics
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Meningococcus = Benzylpenicillin
Everything else = Cefotaxime |
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Meningitis CSF changes
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Bacterial = turbid, low glucose, high protein, mostly polymorphs
TB = fibrin web, low glucose, high protein, mostly lymphocytes Viral = clear/turbid, normalish glucose and protein, mostly lymphocytes |
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Somatic sensory tracts
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1. Dorsal column
2. Spinothalamic tract 3. Trigeminothalamic pathway |
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Dorsal column
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Touch, pressure, vibration, and conscious
proprioception from the limbs, trunk, neck, and posterior head. Made up of the gracile fasciculus (medial), which propagates information from the lower body, and the cuneate fasciculus (lateral), which propagates information from the upper body. Decussate at medulla, cross to medial lemniscus of midbrain. |
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Spinothalamic pathway
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Pain, temperature, itch, and tickle from the
limbs, trunk, neck, and posterior head. Decussate in the spinal column |
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Trigeminothalamic pathway
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Tactile. thermal, and pain sensations from the face, nasal cavity, oral cavity, and teeth. Through the trigeminal nerves.
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Spinocerebellar tracts
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Proprioception from the trunk and limbs to the ipsilateral side of the cerebellum
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Lateral corticospinal
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Decussates at medulla and innervates distal parts of limbs (90% of the corticospinal tract)
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Anterior corticospinal
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Decussates at the spinal cord at the level of exit. Innervates proximal limbs and trunk. Makes up 10% of the corticospinal tract.
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Rubrospinal
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Precise, voluntary movements of the distal part of the upper limbs
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Tectospinal
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Reflexively moves head, eyes, and trunk in response to visual or auditory stimuli
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Vestibulospinal
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Maintains posture and balance in response to head movements
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Reticulospinal
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Ipsilateral skeletal muscles of the trunk, proximal parts of the limbs. Regulates muscle tone in response to ongoing movements.
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Tendon reflex: Biceps - root?
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C5, C6
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Tendon reflex: Brachioradialis - root?
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C6
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Tendon reflex: Triceps - root?
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C7
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Tendon reflex: Patellar - root?
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L4
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Tendon reflex: Achilles - root?
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S1
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Bulbar palsy ('bulb' = medulla)
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LMN weakness of muscles whose cranial nerve nuclei lie in the medulla. Seen in myasthenia gravis, botulism, and dystrophies.
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Pseudobulbar palsy
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UMN lesions of the lower cranial nerves, producing weakness of the tongue and pharyngeal muscles. Seen in MND, MS, cerebrovascular disease, and following a severe brain injury.
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Extradural haemorrhage
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Rupture of the middle meningeal artery. Blood accumulates over minutes/hours. Classically presents with a lucid interval.
Can lead to ipsilateral dilated pupil and contralateral hemiparesis. Respiratory arrest follows. Diagnose with CT. |
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Generalised seizure definition
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Bilateral electrical abnormality with bilateral motor manifestations and impaired consciousness
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Generalised seizure examples
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Petit mal, grand mal, myoclonic
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Partial focal seizure definition
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Electrical abnormality localised to one part of the brain
Simple - without loss of awareness Complex - with loss of awareness |
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Partial focal seizure examples
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Simple = Jacksonian
Complex = Temporal lobe epilepsy |
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Myasthenia gravis
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Weakness of proximal limb, bulbar, and ocular muscles. Heart is not affected. Caused by antibodies to acetylcholine receptor protein antibodies. Treat with oral anticholinesterases and immunosuppressants.
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Guillain-Barre
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Monophasic polyneuropathy. Typically follows gastro infection (CMV and campylobacter). Weakness begins distally and extends proximally (glove and stocking polyneuropathy). Provide supportive care until symptoms resolve (typically around six weeks).
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MS
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Inflammation of CNS (i.e. does not effect peripheral nerves). Steroids for exacerbations, otherwise - beta interferon and azathiprine.
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Becker's muscular dystrophy
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X-linked (therefore, vast majority male). Less severe and less common than DMD. Symptoms appear later on in childhood and early adulthood. Main symptoms are lower limb weakness (frequent falls, Gower's manoeuvre), fatigue, and cardiac disease.
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Duchenne's muscular dystrophy
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X-linked. Muscle destruction due to lack of dystrophin. Symptoms typically appear before age 6. Early signs include pseudohypertrophy of calf muscle. Life expectancy is around 25.
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Friedrich's ataxia
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Progressive degeneration of sensory and motor tacts. Progressive difficulty in walking before age 12, death typically before age 40. Findings typically include ataxia of the gait and trunk, nystagmus, dysarthria, loss of position and vibration sense in lower limb, optic atrophy, pes cavus and cardiomyopathy.
Basically - Ataxia + nystagmus + optic atrophy in a young patient is probably Friedrich's ataxia. |
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Syringomyelia
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A fluid filled cavity in the spinal cord. Cavity expands between C2 and T9, destroying neurones. Lower cranial nerve nuclei destroyed.
Symptoms typically by age 20-30. Typical is upper limb pain exacerbated by exertion or coughing. Loss of pain and temperature sensation. Investigate by MRI T2. Treat, but not cure, with surgical decompression. |
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Side effects of phenytoin
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Sodium channel blocker.
Acute: Dizziness, diplopia, nystagmus, slurred speech, ataxia. Chronic: Gingival hyperplasia, hirsuitism, coarsening facial features, anaemia Idiosyncratic: Fever, rash, hepatitis, dupuytren's contracture, drug induced lupus Teratogenic: Cleft palate, heart disease |
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Sodium valproate
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GABA agonist
Nausea, weight gain, alopecia, pancreatitis, hyponatraemia |
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Carbamazepine
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Sodium channel blocker
Dizziness, ataxia, drowsiness, headache, agranulocytosis |
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Signs of UMN lesion
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Contralateral signs
No fasciculation or muscle wasting Spasticity +/- clonus Weakness, predominantly extensors in the arm and flexors in the leg Exaggerated tendon reflexes Extensor plantar response Pronater drift |
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Signs of LMN lesion
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Ipsilateral signs
Fasciculation and wasting present Hypotonia Loss of tendon reflexes |
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Examples of anterior horn cell lesions
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MND, poliomyelitis
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Most common disease of NMJ
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Myaesthenia gravis
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Weakness abducting arms?
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Deltoid - C5
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Weakness flexing at elbows?
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Biceps - C6
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Weakness extending at elbows?
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Triceps - C7
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Weakness in power grip?
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C8
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Weakness abducting fingers?
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T1
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Weakness flexing at hips?
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Psoas - L1
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Weakness adducting legs?
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L2
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Weakness extending at knees?
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Quads - L3
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Weakness dorsiflexing or inverting feet?
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L4
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Weakness extending or everting feet?
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L5
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Weakness flexing toes?
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S1
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Bladder problems?
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S2
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Symptoms of pontine lesions
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Absolute loss of sensation on the contralateral side
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Symptoms of thalamic lesions
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Absolute loss of sensation on the contralateral side +/- spontaneous pain
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Symptoms of cortical lesions
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Sensory loss and neglect on one side of the body
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Signs and symptoms of a cerebellar lesion
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Ataxic gait
Intention tremor Past pointing Clumsy rapid alternating movements (dysdiadochokinesis) Horizontal nystagmus Dysarthria (halting, jerky speech) Titubation (tremor of the head) |
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Fundamental cause of monocular, bitemporal and homonymous hemianopia, homonymous quadrantanopa visual loss
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Monocular = Damage to the eye or optic nerve
Bitemporal = lesions at the chiasm Homonymous hemianopia = tract (no sparing of central vision), radiation or cortex (both with sparing of central vision) Homonymous quadrantanopia = PITS (parietal lesion leads to inferior loss, temporal lesion leads to superior loss) |
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What is an Argyll Robertson pupil?
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Comically known as a prostitutes pupil as it accommodates but doesn't react (to light). Often seen in neurosyphilis.
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Most frequent cause of third nerve palsy
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Berry aneurysm arising in the PCA
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Signs of sixth nerve palsy
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Inability to abduct the eye beyond the midline due to unopposed action of the medial rectus. Patients complain about worsening diplopia when gazing to the side of the lesion
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Signs of fourth nerve palsy
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Diplopia when attempting to look down and away from the affected side
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Signs of fifth nerve lesion (not trigeminal neuralgia)
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Reduction of corneal reflex. Unilateral sensory loss on face, tongue, buccal mucosa. Jaw deviates to side of lesion when mouth is opened.
A brisk jaw jerk is seen with UMN lesions |
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Management of trigeminal neuralgia
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1. Carbamazepine
2. Carbamazepine + lamotrigine 3. Gabapentin If medical management fails, surgery via microvascular decompression |
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Management of facial nerve lesions
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Typically Bell's Palsy so give prednisolone. If severe, give antivirals (valaciclovir or aciclovir).
If vesicles in auditory canal or on soft palate, diagnosis is Ramsay-Hunt syndrome |
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Explain the difference between bulbar and pseudobulbar palsy in broad terms
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The 'bulb' is the medulla, and the palsy in question is caused by insult to the cranial nerves that run through it (IX-XII).
A bulbar palsy is a weakness of the LMN type, typically caused by MND, syringobulbia, and Gullain-Barre syndrome. Presentation includes dysphagia, dysarthria, and nasal regurgitation. Tongue is wasted and fasciculating. Pseudobulbar palsy is an UMN weakness of the same muscle groups. Typically caused by stroke and MS. Presents with dysarthria, dysphagia, and nasal regurgitation. Jaw jerk is exaggerrated. Tongue is small and spastic with no fasciculation. |
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GCS
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Rated out of 15. Below 8 is considered to be a medical concern due to inability to protect airway.
Three measures - eyes (4), verbal (5), movement (6) Eyes: 4. Open spontaneously 3. Open on command 2. Open to pain 1. Unable to open Verbal: 5. Talking as normal. Oriented. 4. Talking but confused 3. Inappropriate use of words 2. Incomprehensible sounds 1. No audible sounds Movement: 6. Normal. Able to follow commands 5. Limb localises to pain 4. Limb withdraws from pain 3. Limb flexes to pain 2. Limb extends to pain 1. No response |
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Cause of a unilateral, fixed dilated pupil
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Coning
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Cause of bilateral, fixed dilated pupils
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Brain death, deep coma (barbiturate or hypothermia)
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Causes of pinpoint pupils
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Opiates or pontine lesions
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Causes of midpoint pupils
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Coma of metabolic origin or caused by CNS depressant drugs
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Clinical features of SAH
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Sudden, devastating, occipital headache. Vomiting, coma, death. Neck stiffness, positive Kernig's sign.
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IVx SAH
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CT - hyperdense areas. If in doubt, lumbar puncture (CSF becomes xanthochromic (yellow) several hours after SAH).
If fit for surgery, do MR angiography. |
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Complications from SAH (think physical)
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Blood in SA space can lead to obstructive hydrocephalus
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Management of SAH
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Admit to ICU and provide support for BP, HR, etc.
Surgery - clipping or coil embolisation. Nifedipine reduces mortality. |
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Most common bacterial causes of meningitis in UK
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N. meningitidis
S. Pneumoniae S. Aureus Strep B |
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Most common viral causes of meningitis in UK
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ECHO
Coxsackie Polio Mumps Herpes simplex HIV EBV |
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Most common fungal causes of meningitis in UK
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Cryptococcus neoformans
Candida albicans |
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Meningitis signs and symptoms
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Classic triad: Headache, neck stiffness, fever.
Also - photophobia, vomiting, irritability, positive Kernig's sign |
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Clinical clues in meningitis
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Rash? - meningococcal
Skull fracture/ear disease/CNS lesion - pneumococcal Immunocompromised - HIV |
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Treatment of bacterial meningitis
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Post head trauma - vancomycin and ceftriaxone
<1 month old - ampicillin and cefotaxime >1 month <50 years - vancomycin and ceftriaxone >50 years - ampicillin and vancomycin |
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Most common bacterial meningitis by age
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Newborns - group b strep, e. coli, listeria
Children - strep pneumonia, n. meningitidis, haemophilus Young adults - n. meningitidis, strep pneumoniae Old adults - s. pneumoniae, n. meningitidis, listeria |
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Treatment of fungal meningitis
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Amphotericin B + flucytosine or fluconazole
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CSF changes in bacterial, viral and TB meningitis
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Normal - crystal clear, no polymorphs, protein 0.2-0.4 g/L, glucose 2/3 - 1/2 of blood glucose
Bacterial - turbid/purulent, 200+ /mm3 polymorphs, 0.5-2 g/L protein, glucose less than half of blood glucose Viral - clear/turbid, no polymorphs, protein 0.4-0.8 g/L, glucose >1/2 blood glucose TB - fibrin web, 0-200/mm3 polymorphs, 0.5-3 g/L protein, glucose < 1/2 blood glucose |
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Diagnostic criteria of migraine
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At least two of...
- unilateral pain - throbbing type pain - moderate to severe intensity - motion sensitivity And at least one of... - Nausea/vomiting - Photophobia/phonophobia - Normal clinical examination |
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Migraine management
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Analgesics (aspirin, paracetamol, NSAIDs). A triptan (e.g. sumatriptan).
Prophylaxis includes valproate, beta blockers, tricyclics, and botox |
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Typical cluster headache patient
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Male aged 20-40
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Clinical features of cluster headaches
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Recurrent bouts of excruciating retro-orbital pain with parasympathetic trunk activation in same eye causing redness and tearing.
Patients prefer to move rather than sit still as in migraines Attacks typically last 30-90 mins and may occur several times per day |
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Cluster headaches management
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Most analgesics are useless. Subcut triptan is drug of choice.
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Raised ICP management
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Eliminate causal factors
Acetazolamide, furosemide CSF shunt |
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Trigeminal neuralgia management
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Carbamazepine
Adjunct with lamotrigine or topiramate Gabapentin is third line Consider ablative surgery and neurostimulation |
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What is amaurosis fugax
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Transient visual loss in one eye due to the passage of emboli through the retinal artery
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Features of anterior circulation CVAs
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Amaurosis fugax, aphasia, hemiparesis, hemisensory loss, hemianopic loss
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Features of posterior circulation CVAs
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Diplopia, vertigo, vomiting. Choking and dysarthria. Ataxia. Hemisensory loss. Hemianopic visual loss. Bilateral visual loss. Tetraparesis. Loss of consciousness. Transient amnesia.
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What is the ABCD2 score for stroke risk?
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Stratifies risk of having a stroke within 7 days of a TIA
Age > 60 (1 point) BP > 140/90 (1 point) Clinical features - Unilateral weakness (2 points) - Isolated speech disturbance (1 point) Duration of symptoms - >60 minutes (2 points) - 10-59 (1 point) - <10 minutes Diabetes - Present (1 point) - Absent (0 points) |
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TIA Ivx
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Carotid doppler
Cardiac echo CT/MR brain and angiography |
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Left middle cerebral artery neurological deficits in stroke
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Right sided weakness involving face and arm > leg with dysphasia
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Right middle cerebral artery neurological deficits in stroke
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Left sided weakness involving face and arm > leg. Visual and/or sensory neglect, denial of disability.
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Lateral medulla neurological deficits in stroke
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Ipsilateral Horner's syndrome, Xth nerve palsy, facial sensory loss, limb ataxia with contralateral spinothalamic sensory loss. Vertigo. Dysphagia.
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Posterior cerebral artery neurological deficits in stroke
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Homonymous hemianopia. Other deficits due to parietal and/or temporal lobe involvement
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Internal capsule neurological deficits in stroke
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Motor, sensory or sensorimotor loss face = arm = leg. Profound dysa arteryrthria due to involvement of corticobulbar fibres but not dysphasia or other cortical deficits
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Bilateral paramedian thalamus neurological deficits in stroke
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Coma. Opthalmoplegia. Ataxia. Memory impairment. Some require ventilation.
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Carotid artery dissection neurological deficits
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Ipsilateral Horner's syndrome
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IVx of choice in stroke is...
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MRI. If not available, CT
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Historical exclusion criteria for thrombolysis following stroke
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Stroke or head trauma in last 3 months
Prior history of intracranial haemorrhage Surgery within 14 days GI or GU bleeding within 21 days MI in previous 3 months Arterial puncture at a non-compressible site within 7 days LP within 7 days |
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Clinical exclusion criteria for thrombolysis following stroke
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Rapidly improving symptoms
Minor neurological signs Seizure at onset of stroke Symptoms suggestive of SAH Acute MI or post-MI pericarditis Persistent systolic BP >185 Pregnancy or lactation Active bleeding |
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Laboratory exclusion criteria for thrombolysis following stroke
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Platelets < 100,000/mm3
Serum glucose <2.8 mmol/L or >21.2 mmol/L INR > 1.7 if on warfarin Elevated partial thromboplastin time if on heparin |
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How to gibe IV alteplase following stroke
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Dose of 0.9 mg/kg up to 90mg
10% of total given IV over 1 minute Remainder infused over 60 minutes |
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Management of stroke
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Thrombolysis unless contraindicated. If contraindicated, give aspirin 300 mg/day.
If haemorrhage, surgery. |
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Stroke prognosis
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25% die within 2 years. 10% within 1 month.
Mortality higher in haemorrhage than thromboembolic infarction. |
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Define simple and complex partial seizures
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Simple partial = without loss of awareness, e.g. Jacksonian seizure
Complex partial = with loss of awareness e.g. temporal lobe seizure |
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Four types of generalised seizures
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1. Petit mal
2. Grand mal 3. Myoclonic 4. Tonic and atonic |
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Management of status epilepticus
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Lorazepam IV bolus
If seizures persist, IV phenytoin. If phenytoin is contraindicated, give phenobarbitol. No IV access? Buccal midazolam Transfer to ITU if seizures persist for 30 mins |
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First and second line management of grand mal seizures
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First line: Sodium valproate, levetiracetam, lamotrigine, carbamazepine, oxycarbazepine, topiramate
Second line: Phenobarbitol, clobazam, clonazepam, phenytoin |
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First and second line management of focal seizures
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First line: Carbamazepine, lamotrigine, levetiracetam, sodium valproate, oxycarbazepine, topiramate
Second line: Clobazam, gabapentin, pregabalin |
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First and second line management of myoclonic seizures
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First line: Sodium valproate, levetiracetam
Second line: clonazepam, clobazam, lamotrigine Carbamazepine and oxycarbazepine may worsen myoclonic attacks |
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What causes vegetative state?
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Damage to cortex and hemispheres
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What causes locked in syndrome?
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Damage to ventral pons
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Distinguishing features of vegetative state
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Awareness is absent
Sleep-wake cycles are present Response to noxious stimuli E4, M1-4, V1-2 No purposeful movement Preserved respiration Slow waves on EEG |
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Distinguishing features of locked in syndrome
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Awareness is preserved
Sleep-wake cycle is preserved Only response of any sort is via eyes (vertical movement) E4, V1, M1 Respiration preserved EEG normal |
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Epidemiology of MS
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Women > men, age 20-40, distance from equator (white folk)
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Pathogenesis of MS
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T cell mediated autoimmune disease causing inflammatory process within white matter of brain and spinal cord. Result in plaques of demyelination. Affects CNS rather than PNS
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Three main clinical patterns in MS
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Relapsing-remitting (90%). Onset over days, recovery over weeks. Average of one relapse per year.
Secondary progressive MS. Follows relapsing-remitting in 75% of cases, typically after 35 years, and is late stage. Primary progressive (10%). Gradually worsening disability without relapses or remissions. Associated with fewer inflammatory changes on MRI. |
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Clinical presentation of MS
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Optic neuritis (colour desaturation).
Brainstem signs - diplopia, vertigo, facial numbness/weakness, dysarthria, dysphagia. Spinal cord signs - paraparesis developing over days or weeks Late MS causes spastic tetraparesis, ataxia, optic atrophy, nystagmus, brainstem signs, pseudobulbar palsy, and urinary incontinence. |
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IVx of MS
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MRI brain and cord.
CSF shows oligoclonal bands in 90% of cases but these are not diagnostic Visual evoked responses |
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MS management
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MDT essential. Short courses of methylprednisolone for relapses.
Beta interferon and glatiramer acetate reduce relapse rate by one third. Offer after 2 significant relapses over a 2 year period or 1 disabling relapse. |
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Poor prognostic signs in MS
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High MR lesion load, high relapse rate, male gender, late presentation.
Life expectancy reduced by 7 years on average |
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Clinical effects of cerebellar lesions
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Ipsilateral weakness. Wide based or ataxic gait. Nystagmus. Disturbances of muscle tone and axial and truncal control. Delays in starting and stopping movements, tremor, poor coordination.
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Gross motor function classification system for CP (grades 1-5)
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1. Unimpaired except for advanced gross motor skills.
2. Walks mostly without assistive devices. Rails for stairs, difficulty on uneven ground. 3. Walks with assistive devices. Wheelchair for long distances. 4. Limited mobility. Wheelchair or power chair is primary tool for mobility. May walk for short distance with assistance. 5. Total dependence. |
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Epidemiology of PD
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1 in 200 over age of 80. M:F = 1.5:1
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Pathology of PD
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Lewy bodies + loss of dopaminergic neurones from pars compacta of the substantia nigra of the midbrain (project to striatum of the basal ganglia)
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Premotor symptoms in PD
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Anosmia, depression, aches/pains, REM sleep disorder, autonomic features (urinary urgency, hypotension), constipation, restless leg syndrome
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Motor symptoms in PD
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Tremor (70% presenting symptom. Spreads to leg on same side then arm on other side), rigidity (lead pipe), akinesia, postural disturbance.
Impassive face. Micrographia. |
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IVx PD
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Clinical. Refer.
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PD management
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Levodopa plus carbidopa to reduce peripheral symptoms. Domperidone to prevent N&V.
Consider selegiline or rasagiline. If advanced, consider amantidine to improve dyskinesia. |
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Ivx for Huntington's
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CAG repeat (diagnostic)
MRI - may show changes |
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Management of Huntington's
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Symptomatic. No disease modifying drugs at present.
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MND is also known as...
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ALS (amyotrophic lateral sclerosis)
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% with cognitive impairment in MND
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40%. 5% have dementia.
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Sensory symptoms of MND
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None
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Classic presentation of MND/ALS
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Progressive focal muscle weakness and wasting with fasciculations. Examination reveals brisk reflexes.
MND features UMN and LMN symptoms Brisk reflexes + wasting = MND |
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Classic presentation of progressive muscle atrophy in MND
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Pure LMN presentation. Weakness, wasting, fasciculation.
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Classic presentation of progressive bulbar and pseudobulbar palsy (20%) in MND
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Dysarthria, dysphagia, nasal regurgitation.
Mixed bulbar palsy shows fasciculating tongue with slow, stiff movements. Pseudobulbar palsy may present with emotional incontinence (pathological laughter and/or crying) |
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Presentation of primary lateral sclerosis in MND (1-2%)
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The least common form. Presents with UMN signs only. Causes slow progressive tetraparesis and pseudobulbar palsy.
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How do gliomas spread?
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Direct extension, very rarely metastasise outside the CNS
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What is Guillain-Barre syndrome?
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A demyelinating polyneuropathy, classically ascending. Typically following gastroenteritis or influenza-like illness. Characterised by motor difficulty, absence of deep tendon reflexes, paraesthesia without objective sensory loss, increased CSF albumin.
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Guillain-Barre IVx
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Nerve conduction studies, raised CSF protein with normal cell count and glucose count, antibodies against GQ1b
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Guillain-Barre management
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Respiratory support, plasma exchange, IV immunoglobulin
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Presentation of radial nerve palsy
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Wrist drop
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Presentation of median nerve palsy
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Ape hand deformity (loss of ability to abduct and oppose thumb)
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Presentation of ulnar nerve palsy
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Hand of benedict
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Definition of myaesthenia gravis
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Chronic autoimmune disorder of the post synaptic membrane at the neuromuscular juntion (NMJ)
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Presentation of myaesthenia gravis
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Muscular weakness with fatiguability. Proximal limb muscles, extraocular, speech, facial expression, and mastication muscles are commonly affected.
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IVx of MG
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Serum anti-AChR and anti-MuSK antibodies
Repetitive nerve stimulation shows decrement in the muscle action potential |
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MG management
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Pyridostigmine (anticholinesterase)
Steroids Thymectomy IV immunoglobulins |
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Definition of Duchenne muscular dystrophy and Becker's muscular dystrophy
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DMD features absence of dystrophin, Becker's features present but low levels of dystrophin. Condition is X linked recessive so patients are almost all BOYS.
DMD is more severe, clinically apparent by age 4 and often causes death by age 20. Becker's becomes apparent in young adults. |
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Clinical features of DMD
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Proximal limb weakness with calf pseudohypertrophy. Gower's sign (using hands to climb up legs to stand up) is present. Myocardium is affected.
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Investigation of DMD
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Clinical diagnosis + elevated CK + variation in muscle fibre size and replacement by fat on biopsy
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Cutaneous features of tuberous sclerosis
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Depigmented 'ash-leaf' spots - fluoresce under UV light
Roughened patches of skin over lumber spine (Shagreen patches) Adenoma sebaceum (butterfly distribution over nose) Subungual fibromata Cafe-au-lait spots |
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Neurological features of tuberous sclerosis
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Developmental delay
Epilepsy Intellectual impairment |
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Non cutaneous or neurological features of tuberous sclerosis
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Retinal hemartomas (dense white areas on retina)
Rhabdomyomas of the heart Gliomatous change in brain lesions Polycystic kidneys, renal angiomyoliopomata |
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Management of BP during stroke
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Don't attempt to lower unless there are complications e.g. hypertensive encephalopathy
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Management of AF following stroke
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Don't restart anticoagulants for 14 days
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Drug management following stroke
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If cholesterol >3.5, start a statin. Clopidogrel unless contraindicated, in which case use MR dipyridamole.
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