Session 8: Neurology and Stroke Flashcards Preview

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Flashcards in Session 8: Neurology and Stroke Deck (26):
1

Describe possible localisations of injury (can be applied to pattterns sensory loss as well)

    Brain (post-central gyrus – somatosensory cortex)

     Brainstem   

   Cerebellum

    Spinal Cord

    Anterior (ventral) Horn Cell (motor neurone diseases)

    Nerve Roots (acute polyradiculoneuropathies)

    Nerve (acute neuropathies)

    Neuromuscular junction

    Muscle (acute myopathies)

    Other

   Functional

    Consider if its CNS/PNS

    NEED TO LEARN DERMATOMES

2

What are upper motor neuron (pyramidal) signs?

    Increased tone: spasticity (velocity-dependent; a ‘catch’ during fast extension of the elbow or fast supination of the forearm indicates spasticity – clasp knife) or rigidity (velocity independent, increased tone throughout a range movement, associated with basal ganglia disorder (extrapyramidal sign), can be lead pipe or cogwheeling, sometimes associated with tremor).

    Reduced power or loss of dexterity; pyramidal distribution of weakness (U/L: flexors stronger than extensors, L/L: extensors stronger than flexors)

    Pronator drift

    Brisk reflexes (due to hyperactive stretch reflexes) +/- clonus

    Extensor Plantars (Hoffman’s Sign/Babinski Sign)

  • Hoffman’s Sign: flick terminal phalanx (hyper-extend) of the middle or ring finger=> reflex spreads pathologically (flexion of the terminal phalanx of the thumb is seen).
  • Babinski Sign: extensor plantar response + fanning of toes (meant to use a painful stimulus)

3

What are lower motor neurone lesion signs?

    Wasting and fasciculation (affected proximal part of LMN) (spontaneous electrical activity in single motor units – pathologically large – due to process of denervation and attempted repair)

    Reduced tone

    Weakness: pattern of weakness points to different anatomical regions

    Reduced or absent reflexes 

4

Give some pattern of weakness examples

Nerve root e.g. prolapsed disc

Mononeuropathy e.g. median nerve

Polynueropathy: distal patterning of weakness + sensory loss (glove and stocking syndrome); length-dependent (longest nerves affected earliest)

Widespread e.g. (anterior horn cell disease – MND)

Further examples:

  • Pareparesis: strongly suggests spinal cord problem
  • Hemiparesis e.g. due to stroke
  • Monoparesis (e.g. due to brachial plexopathy, lumbar plexopathy, stroke)
  • Quadriparesis/tetraparesis e.g. multiple sclerosis, muscular dystrophy (damage to the brain or the spinal cord at a high level C1-C7) 

5

Revise Dermatomes and Cutaneous Nerves

Revise Dermatomes and Cutaneous Nerves!!!

Inguinal ligament = approx T12

6

Recap the Corticospinal Tracts

    decussates in inferior part of medulla (at medulla oblongata in brainstem)

  • Anterior fibres stay on same side
  • Lateral fibres (majority of corticospinal tract) cross in pyramids of medulla

Neurones come from the motor cortex (pre-central gyrus), premotor and parietal lobe regions of the brain.

7

Describe the Dorsal Columns

Fasciculus gracilis and fasciculus cuneatus

Involved in proprioception and fine touch

(Discriminative touch receptor (f.Gracilis) or proprioceptor (f.Cuneatus) in the periphery => 1st order sensory neurone => 1st order neuron in f.Gracilis and f.Cuneatus tracts reach medulla oblongata => fibres cross in medulla => axons of 2nd order neurones in the medial lemniscus => thalamus receives all conscious sensations => third order neurones to cerebral cortex => Cerebral cortex: to perceptive areas for touch and proprioception

8

Describe the Spinothalamic Tract

Crude touch, pain and temperature

Cross at spinal cord 

9

What is the Artery of Adamkiewicz?

In injuries informing the anterior spinal artery, dorsal columns get spared (due to blood supply from posterior spinal artery)

The Artery of Adamkiewicz is the largest anterior segment medullary artery (branch of the anterior spinal artery).

    When damaged or obstructed, it can result in anterior spinal artery / anterior cord syndrome with loss of urinary and fecal continence and impaired motor function of the legs; sensory function is often preserved to a degree.

    It is important to identify the location of the artery when surgically treating an aortic aneurysm to prevent damage, which would result in insufficient blood supply to the spinal cord. Its location can be identified via CT.

10

Describe the Posterior Spinal Artery

arises from the vertebral artery, adjacent to the medulla oblongata, reinforced by a succession of segmental branches along its pathway to form a plexus called the vasocorona. The posterior spinal arteries are seen as rather larger longitudinal channels of an extensive pial arterial meshwork – compared to the anterior spinal artery, which can be traced as a distinct channel throughout its course.

    Branches from the posterior spinal arteries form a free anastomosis around the posterior roots of the spinal nerves.

    It rarely gets occluded – Posterior Cord Syndrome is very rare. Clinical presentation includes loss of proprioception + vibration sense + loss of two point discrimination + loss of light touch.

11

What is meant by glove and stocking?

    length – dependent – longest nerves affected first

    polyneuropathy or symmetrical polyneuropathy is damage or disease affecting peripheral nerves (peripheral neuropathy) in roughly the same areas on both sides of the body, featuring weakness, numbness, pins-and-needles, and burning pain. It usually begins in the hands and feet and may progress to the arms and legs; and sometimes to other parts of the body where it may affect the autonomic nervous system. It may be acute (appearing suddenly, progressing rapidly and resolving slowly) or chronic (emerging and developing gradually). A number of different disorders may cause polyneuropathy, including diabetes and some types of Guillain-Barré syndrome.

12

What are cerebellar signs? What is Romberg's test actually testing for?

Cerebellar Signs

  •     Broad-based ataxic gait
  •     Nystagmus (spontaneous, jerky eye movements)
  •     Dysarthria (slurred speech – scanning or explosive)
  •     Finger-Nose ataxia (dysmetria, past-pointing, intention tremor) NB: examiner needs to make sure patient is fully extending their arm
  •           Dysdiadochokinesia 
  •     Heel-shin ataxia

Romberg’s Sign

  •     Differentiates between sensory and cerebellar ataxia
  •     Compares degree of unsteadiness with eyes closed versus eyes open
  •     If significantly more unstead when eyes closed => Positive Romberg’s Sign => Sensory ataxia (proprioceptive deficit)

13

What is a stroke?

Stroke: a sudden onset of focal neurological deficit from a vascular cause i.e. in a vascular territory

    Two types: ischaemic and haemorrhagic but lots of subsets such as thromboemboliv, primary/secondary haemorrhage etc

14

What are the risk factors for stroke?

    Modifiable:

  • Blood pressure
  • Diabetes
  • Cholesterol
  • Smoking / excess alcohol
  • Obesity / lack of exercise
  • Atrial fibrillation
  • Hyper-coagulable states
  • Drug abuse (cocacine0
  • Infections
  • Legal highs

   Unmodifiable

  • Male gender
  • Increasing age
  • Family history

    Sometimes no cause is found (cryptogenic stroke = 10% of all strokes)

15

What is an Ischaemic Stroke? What is meant by the penumbra?

Ischaemic stroke: blood clot stops the flow of blood to an area of the brain (infarct).

    Two major zones of injury: the core ischaemic zone and the “ischaemic penumbra” (the term generally used to define ischaemic but still viable central tissue.

    Brain cells within the penumbra, a rim of mild to moderately ischaemic tissue lying between tissue that is normally perfused and the area in which infarction is evolving, may remain viable for several hours. This is because the penumbral zone is supplied with blood by collateral arteries anastomosing with branches of the occluded vascular tree. However, even cells in this region will die if reperfusion is not established during the early hours since collateral circulation is inadequate to maintain the neuronal demand for oxygen and glucose indefinitely.

16

What are the types of ischaemic stroke?

    Thrombus in situ (atheroma) i.e. small vessel disease

    Embolic – common in AF, valvular diseases such as mitral valve, rheumatic fever

  • Cardiac
  • Large artery (neck or aortic arch)

    Rarities e.g. HIV related (accelerates atherosclerosis), vasculitis (rheumatoid arthritis lupus), bacterial endocarditis, hypercoagulable state due to pregnancy or cancer.

    It is conceivable that a Patent Foramen Ovale could lead to stroke but clinically only happens during women given birth (Valsalva’s manoeuvre increases right => left flow of blood). 

17

Describe thrombolysis therapy

    At best 15% stroke patients eligible – contraindications include high blood pressure, present too late, great risk of haemorrhage/bleeding etc

    NOT the be all and end all

    Emphasis is on multi-disciplinary care (stroke unit teams) – good nursing care and physiological parameter control are as if not more important and apply to everyone.

    rTPA (recombinant TPA is used)

  • 0-4.5 hours within onset. ‘Time is brain’.
  • CT criteria and NIHSS (NIH Stroke Scale) scores neurological deficit – can be used to track progress.
  • Bleeding risk associated with treatment
  • Consider biological age vs chronological age and function
  • Contraindications e.g. post-operation, arterial puncture in groin
  • 0.9mg/kg. 10% bolus then rest over 60 mins infusion.
  •     NB: NNT =number needed to treat

18

What is a possible treatment option of stroke in the future?

Thrombectomy is a potential treatment option in the future

    Potential for mechanical extraction within first 6 hours

    Lack of specialised interventional neuro-radiologists.

    Can the NHS cope with the financial cost? Is it ethically justifiable?         

19

What is meant by secondary prevention?

Secondary Prevention

  •     Depends on underlying cause
  •     Antithrombotic therapy vs anticoagulation. Also consider Novel Oral Anticoagulants!
  •     BP (aim for
  •     Lipid control
  •     Sugar control
  •     Lifestyle – can be difficult to get them to give up smoking if they are very disabled (need to think about quality of life)
  •     Carotd endartectomy (surgery to unblock a carotid artery).

NB: scan shows lobar bleed – potentially secondary bleed rather than primary.

20

What is a haemorrhagic stroke?

Haemorrhagic Stroke: weakened/diseased blood vessels rupture – commonly due to hypertension. Blood leaks into brain tissue

    Types of haemorrhagic stroke

  • Primary bleed usually hypertensive
  • Secondary due to anticoagulation
  • Underlying vascular abnormality
  • Underlying tumour
  • Cerebral amyloid angiopathy (ageing of the brain – linked with disability and dementia, can lead to both ischaemic and haemorrhagic events)

    Secondary prevention

Blood pressure, lifestyle etc

Exclude underlying cause

21

What do the symptoms depend on?

Symptoms depend on lobes and blood vessels involved. The cerebellum can also be affected.

Note for graphic: green = ACA, red = MCA, blue = PCA. Superficial (cortical) “watershed zone”  = confluence of 3 territories.

22

What is the OCSP Classification?

OCSP (Oxford Community Stroke Project) Classification: 4 clinical-based subtypes recognised

  •     Total anterior circulation syndrome (TACS): hemiparesis, heisensory loss, hemianopia and higher cortical dysfunction. Worst prognosis - 60% dead at 12 months. Underlying cause is usually cardiac emboli.
  •     Partial anterior circulation syndrome (PACS) – think carotid artery disease until proven otherwise: two of the above or higher cortical dysfunction only. 4% dead at 12 months. Underlying cause is usually large vessel disease e.g. carotids
  •     Lacunar syndrome (LACS): pure motor, pure sensory  (small artery disease – tiny bit of white matter affected) – only 2% will be dead at 12 months. Underlying cause is usually small vessel disease i.e. atheroma in situ
  •     Posterior circulation syndrome (POCS): posterior circulation event (so brainstem, cerebellum could be affected) – 7% will be dead at 12 months. Can be anything

23

What does the ACA supply and so what possible deficits could arise?

    Motor cortex (controls movement of the contralateral lower limb)

    Sensory cortex (receives sensory input from the contralateral lower limb)

    Supplementary Motor Area (Dominant Hemisphere): functions with Broca’s area in the initiation of speech

    Prefrontal Cortex: functions in volition, motivation, and planning and organising of complex behaviour.

    Left ACA stroke deficits: right leg UMN neuron weakness due to damage to motor cortex and right leg cortical sensory loss due to damage to sensory cortex. Grasp reflex, frontal lobe behavioural abnormalities and transcortical aphasia (language disorders) can also be seen if the prefrontal cortex and supplementary motor areas are involved.

    Right ACA stroke deficits – as well the vice versa of the above, can also include left hemineglect if the prefrontal cortex and non-dominant association cortex are involved (but hemineglect is also seen in MCA strokes).

    ACA infarcts are rare because of the collateral circulation provided by the anterior communicating artery. 

24

What does the MCA supply?

Middle Cerebral Artery supplies

    Broca’s area: expressive speech area, integration with other language areas

    Wernicke’s area: receptive speech area, integration with other language areas

    Motor cortex: movement of contralateral head, neck, trunk and arms

    Sensory cortex: sensation from contralateral head, neck, trunk and arms

    Globus pallidus (site of origin of output from the basal ganglia to substantia nigra and thalamus – functions in the direct and indirect pathways for the initiation and control of movement).

    Internal capsule (anterior limb) contains corticopontine and thalamocortical fibres

    Internal capsule (genu) contains descending fibres of the corticobulbar tract

25

What are the possible deficits in an MCA stroke?

    MCA is the most common site of stroke. Infarcts occur in two general regions: superficial divisions and lenticulostriate branches. Symptoms include

Left MCA superficial division: right face and arm UMN weakness due to damage to motor cortex, non-fluent (Broca’s) aphasia. May also be right face and arm cortical type sensory loss if sensory cortex is involved. Other deficits include a fluent Wernickes aphasia.

Right MCA superficial division: contralateral upper-motor weakness and cortical typ sensory loss, left hemineglect (variable) due to damage to non-dominant association areas.

MCA Lenticulostriate branches: contralateral pure upper-motor hemiparesis due to damage to the basal ganglia (globus pallidus and striatum) and the genu of the internal capsule. Larger infarcts extending to cortex may produce cortical deficits such as aphasia.

26

What does the PCA supply and possible deficits?

Posterior Cerebral Artery supplies (superficial and deep branches):

    Occipital lobe: primary and secondary visual areas, functions in the sensation and interpretation of visual input

    Splenium of corpus callosum: carries commissural fibres connecting right and left visual association cortices.

    Thalamus: relay centre for descending and ascending information. Functions in the integration between cerebral cortex and the rest of the central nervous system.

    Internal capsule (posterior limb): contains descending fibres of the lateral and ventral corticospinal tracts.

    Left PCA deficits: right homonymous hemianopsia due to damage to left visual cortex in the occipital lobe, alexia (inability to recognise or read written words or letters) if splenium of the corpus callosum is affected, infarcts involving the internal capsule and thalamus may cause right hemisensory loss and right hemiparesis.

    Right PCA deficits: left homonymous hemianopsia, left hemisensory loss and hemiparesis