session 7- stroke and neurology Flashcards Preview

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Flashcards in session 7- stroke and neurology Deck (27):

What is paraperesis?

Weakness of both legs 


Lesions of the nervous system at different levels/locations are likley to cause different symptoms. 

What might be features of lesions in the following locations?

  • Brain (left/right)
  • Brainstem 
  • Cerebellum 
  • Spinal cord 
  • Nerve roots 

  • Brain (left/right)
    • If lesion in brain then affects opposite side of body 
    • Can be personality change, problem with higher cognitive function, optic pathway etc. 
  • Brainstem 
    • Can cause cerebellar connection problems or cranial nerve lesions 
  • Cerebellum 
    • Cerebellar lesions have typical signs: DANISH
  • Spinal cord 
    • Small so a lesions is likely to affect both sides of the cord and so both sides of the body
  • Nerve roots (acute polyradiculoneuropathies)
    • Problems seen in a dermatomal/myotomal distribution
    • If nerve roots squashed this can be painful e.g. shooting pain in distribution of the nerve 


What might lesions in the following locations lead to?

  • Peripheral nerves
  • Neuromuscular junction 
  • Muscle 

  • Peripheral nerves 
    • Will be in distribution of the nerve (not dermatome)
    • Drugs, drink + DM are common causes or peripheral neuropathy (can affect more than one peripheral nerve and is likley to affect the feet and hands first- glove and stocking distribution
  • Neuromuscular junction (myasthenia gravis)
    • --> fatigueability but not sensory problems
  • Muscle (acute myopathies)
    • no sensory problems. Often muscles have proximal problems e.g. can't walk upstairs, can't lift arms


What patterns of weakness are seen in lesions in the following areas?

  • Spinal cord
  • Peripheral nerve
  • Nerve roots 
  • Muscle

  • Spinal cord
    • sensory + motor loss below the level of the lesions 
    • If complete transection then there is complete loss on both sides
  • Peripheral nerve
    • If polyneuropathy
      • Show sensory and motor loss/weaknes in glove and stocking distribution 
    • Mononeuropathy
      • signs depend on the nerve affected
  • Nerve roots 
    • sensory/motor loss in the dermatom/myotome affected 
  • Muscle
    • Often shows peripheral muscle weakness (around shoulders + thighs)


What dermatomes are the umbilicus and nipples at?

  • Nipples- C5
  • Umbilicus- T10

N.B. signs at T10 mean the lesion is above this point. The lesion might be a long way above --> false localising signs


What is the blood supply to the posterior and anterior spinal cord? Which tracts are found in these areas?

  • Posterior cord --> paired posterior spinal arteries
    • Dorsal column medial lemniscal tract 
      • Cross at the level of the brainstem so cord lesions affecting these tracts affect the same side of the body (ipsilateral)
  • Anterior cord --> supplied by midline anterior spinal artery 
    • Spinothalamic tract 
      • cross at level of entry of the primary afferent nerve to the spinal cord so effects seen on opposite (contralateral) side to lesion 
    • Lateral corticospinal tract

N.B. signs from spinothalamic seen contralaterally BUT dorsal column seen ipsilaterally - seeing signs on both sides like this is known as dissociated symptoms 


What is the artery of Adamkiewicz?

  • Feeds into the anterior spinal artery 
    • If damaged (e.g. in lower thoracic surgery or aortic aneurysm repair, compression of haemorrhage/embolus) --> spinal cord lesion 
      • Would damage supply to anterior spinal cord 
        • --> affects the corticospinal and spinothalamic tracts 


What are upper motor neurone signs?

  • Increased tone 
  • Reduced power or loss of dexterity 
  • Increased reflexes +/- clonus 
  • Extensor plantars
  • In subtle cases can --> clumsiness rather than obvious weakness 

you don't need all the signs to diagnose UMN lesion just some of the signs in the right context 


What are lower motor neurone signs?

  • Wasting and fasciculation 
  • Reduced tone
  • Weaknes
  • Reduced or absent reflexes 


What are cerebellar signs?

  • Broad based ataxic gain 
  • Nystagmus
  • Dysarthria
  • Finger-nose ataxia
  • Dysdiadochokinesia 
  • Heel-shin ataxia


What is Rombergs sign?

  • Can help determine whether there is sensory or cerebellar ataxia
  • You compare degree of unsteadiness with the eyes closed vs with them open


Alcohol can cause increased ADH production, what does this lead to?

  • NADH
    • Can enter electron transport chain to generate energy
    • Can lead to metabolic disorders:
      • fatty liver, hyperlipidaemia, hypoglycaemia, hyperlactacidaemia, hyperuricaemia, gout sttacks, increased collagen and scar formation 
  • Acetaldehyde
    • Deactivation of proteins, increased collagen, inhibited DNA repair --> mutations and cell death, impairment of electron transport chain


Alcohol can lead to cytochrom p450 induction, what can this lead to?

  • Disturbances in lipid and fatty acid metabolism 
  • Oxygen deficits 
    • cell + tissue damage and less energy production from NADH
  • Oxidative stress
    • e.g. reactive O2 species, depletion of glutathione + activation of substances that can damage the liver and/or cause cancer 


Alcohol can cause primary or secondary malnutrition. What vitamin deficiencies are associated with alcohol?

  • Riboflavin 
    • clinical symptoms are rare
    • Deficiency caused by decreased dietary intake 
  • Folic acid 
    • Causative factors: decreased food intake, malabsorption, decreased hepatic retention, altered enterohepatic recirculation 
  • Ascorbic acid 
  • Vitamine B12 and 6
    • Decreased dietary intake 
    • also alcohol damages the liver and so less cytochromes available to metabolise the vitamins that are eaten


What are the different neurological conditions that alcohol can cause?

  • Intoxication 
  • Abstinence/withdrawal --> hallucinations, delirium tremens (rapid onset confusion)
  • Nutritional diseases:
    • Wernicke/korsakoff syndrome 
    • Alcoholic polyneuropathy 
    • Optic neuropathy 
    • Pellagra 
  • Uncertain pathogenesis 
    • Cerebellar degeneration 
    • Marchiafava-Bignami disease 
    • Osmotic demyelination syndrome 
    • Alcoholic myopathy and cardiomyopathy 
    • Alcoholic dementia 
  • Effects of cirrhosis and portosystemic shunts:
    • Hepatic stupor and coma 
    • Chronic hepatocerebral degeneration 
  • Trauma 


10-30% of alcholics get alcoholic polyneuropathy. What is it and how does it present? How is it investigated and what are symptoms?

  • It causes smal fibre axonal loss 
    • (as opposed to thiamine deficinecy --> large fibre axonal loss)
  • It is sensory, slowly progressive + involves mainly superficial sensation with pain/burning 
    • thiamine def causes motor impairment + deep and superficial sensation impairment 
  • Clinical presentation:
    • symmetrical sensory and motor neuropathy 
    • Asymptomatic
    • Pain, numbness, burning feet, hyperaesthesia 
    • Muscle weakness, dimished reflexes
    • Autonomic involvement 
  • Investigations
    • MCV, nerve conduction studies
  • Prognosis
    • Can recover with alcohol abstinence but slowly 


What is pellagra?

  • Caused by niacin (vit B3) deficiency
    • this is needed for most cellular processes
  • Characterised by diarrhoea, dermatitis + dementia 
    • If left untreated ==> death


A stroke is a sudden onset of focal neurological deficit from a vascular cause. What are the 2 types? 

  • Ischemic 
    • Shows dark areas on CT (cells dying due to lack of blood supply)
    • Types of ischemis stroke:
      • Thrombus forms in situ (atheroma)- small vessel disease
      • Embolic: cardiac or large artery (neck (carotids) or aortic arch)
  • Haemorrhagiv
    • Appears white on CT as lots of blood
      • white on CT= blood, bone, calcification 
    • caused by weakened/diseased blood vessles rupturing 
    • types of haemorrhagic stroke:
      • Primary (due to hypertension)
      • Secondary (due to anticoagulation)
      • Underlying vasc abnormality e.g. AV malformation, dural fistula
      • Underlying tumour 
      • Cerebral amyloid angiopathy (seen in older people)
        • due to amyloid protein plaques (like in Alzheimer's but different parts of brain) and can present with bleeds 


What are modifiable risk factors for stroke?

  • Blood pressure 
  • Diabetes
  • Cholesterol 
  • Smoking/excess alcohol 
  • Obesity/lack of exercise
  • Atrital fibrillation 
  • Hypercoaguable states 
    • If blood too thick --> ischemia 
    • Too thin --> haemorrhagic 
  • Drug abuse (coke stroke) 
  • Infections


What are unmodifiable risk factors for stroke? What are cryptogenic strokes?

  • Unmodifiable risk factors
    • male gender
    • increasing age (biggest RF)
    • Fam history e.g young stroke (<60), cardiovascular disease
    • Ethnicity (different types more common in different ethnicities)
  • Cryptogenic is no cause is found 
    • 10% of all strokes 


What is the OSPC classification of strokes?

  • TACS
    • total anterior circulation stroke
    • due to problem with internal carotid (probs cardiac emboli)
    • --> hemiparesis, hemisensory loss, hemianopaia, higher cortical dysfunction 
    • within 30days, 30% dead, 5% return home, after 12w only 5% who went home will still be alive
  • PACS
    • partial anterior circulation stroke 
    • 2 of symptoms above or higher cortical dysfunction only 
    • due to internal carotid artery 
  • LACS
    • Lacunar stroke syndrome 
    • can be pure motor or pure sensory or mixed 
    • due to internal carotid problem 
      • normally small vesssel disease e.g. atheroma in situ
  • POCS
    • posterior circulation event 
    • vertebral artery problem (e.g. emboli, small or large vessel disease)


When is thrombolysis used in ishcemic strokes?

  • Only 15% are eligible
    • (never give in haemorrhagic as makes it worse)
  • MDT care on a stroke wrad is more important
    • good aftercare is biggest advancement in stroke treatment and in being able to stabilise patients and help them gain independence, not thrombolysis 


What is rTPA?When is it given?

  • rTPA = tissue plasminogen activator (thrombolyssi) 
    • Given 0-4.5 hrs post-ischemic stroke
    • Must do CT first (to check isn't haemorrhagic) +NIHSS scroe (quantifies impairments caused by stroke)
  • Contraindications:
    • Advanced age (can base on biological rather than chronological age), mild or improving stroke symptoms, severe stroke and coma, recent major surgery, recent GI or genitourinary haemorrhage, recent MI 


What is the outcome of rTPA if given at 0-3 hours? What about at 3/4.5hrs?

  • 0-3hrs 
    • 1/3rd better
    • 1/8 nearly normal 
    • 1/20 are worse
  • 3-4.5.hrs 
    • 1/8 better
    • 1/14 nearly normal
    • 1/22 are worse

Highlights importance of early treatment 


In addition to thrombolysis what else can be done in the management of ischemic strokes?

  • Thrombectomy 
    • Not all patients are suitable- this is a new treatment 
    • rankin score is from 0-6 (0= fit and well, 6= dead) 
      • Thrombectomy has been shown to increase the no. of people with scores of 1,2 or 3
      • Can be done for clots in the internal carotid artery and middle cerebral artery
  • Craniotomy 
    • Can prevent death but --> disability 
    • In older patients there is brain shrinkage so room for expansion BUT in young increase in pressure --> midline shift, compression of ventricles etc. 
    • Cardiotomy done in <60yrs (bit of skull removed) --> decrease pressure 
      • the stroke is still there it just helps reduce death from raised ICP (doesn't help quality of life tho)


What can be done for secondary prevention of ischemic strokes?

  • Depends on underlying cause:
    • Anti-platelet vs anticoagulation 
      • e.g. warfarin, heparin, DOACs
    • BP control 
    • Lipid lowering 
    • blood sugar control 
    • Lifestyle 
    • CEA (carotid endarterectomy) 


What is involved in the management of and secondary prevention of haemorrhagic strokes?

  • Reverse anticoagulation e.g. take off warfarin, DOACs
  • Secondary prevention 
    • BP
    • Exclude underlying cause 
      • may need another scan to look for underlying cause after 6-8weeks as this is how long it takes for blood to disappear (before this all u see is blood)