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Integrative > Nervous System Disorders > Flashcards

Nervous System Disorders Flashcards

1
Q

What part of the nervous system is affected in poylradiculoneuropathies?

A

Multiple nerve roots

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2
Q

What is the classic gait which occurs in hemiparesis due to stroke?

A

Circumductive

Arms flexed, finger flexed, legs extended

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3
Q

Contrast spasticity and rigidity.

A

Spasticity = velocity dependent (the faster the limb is moved, the greater the extent of rigidity due to overactive stretch reflex)

Rigidity = non-velocity dependent (limb had lead pipe rigidity regardless of speed of movement; indicates problem is in basal ganglia e.g. Parkinson’s)

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4
Q

What is clonus? How is it detected? How many beats is considered abnormal when testing ankle clonus?

A

Sustained clonic (to and fro) contractions across a joint

Stretching of gastrocnemius by dorsiflexing the foot

Over 2 beats is abnormal

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5
Q

What is Babinski’s sign? Why is it abnormal?

A

Extensor plantar response + fanning of the toes

This pushes the foot towards the pain stimulus instead of away

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6
Q

What is Hoffman’s sign?

A

Flick finger (hyperextension)

Normal = flexing of finger only

Abnormal = flexing spreads to other fingers/thumb

note: same principle applies when testing tendon reflexes

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7
Q

What is the pathophysiology of fasciculations?

A

Individual neurones supply a greater no. of muscle fibres (as some of the nerves are non-functional due to LMN lesion)

AND spontaneous APs occur (attempt to repair damage)

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8
Q

What muscle wasting occurs in ulnar nerve damage or TI nerve root damage?

A

Wasting of dorsal interossei muscles

Causes “guttering” (loss of first dorsal interossus - between thumb and index finger)

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9
Q

Describe the patterns of weakness and sensory loss in different LMN lesions.

A

Nerve root lesion (e.g. prolapsed disc):

  • dermatomal loss of sensation
  • myotomal pattern of weakness

Mononeuropathy (e.g. median nerve in carpal tunnel syndrome):

  • peripheral nerve territory sensation lost
  • specific muscles lost

Polyneuropathy (e.g. diabetic neuropathy):
- long nerves affected first (nerves supplying the hands and feet), causing distal loss of sensation (“glove and stocking” distribution)

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10
Q

Describe the patterns of weakness and loss of sensation in different UMN lesions.

A

Spinal cord level lost (e.g. trauma) = paraparesis

Cortical problem (e.g. stroke) = hemiparesis 
(OR half of spinal cord lost)

+ diffuse indicates motor neurone disease

+ causes of weakness in one leg only could be hemicord syndrome, lumbosacralotomy, or parasagittal (next to spinal cord) lesion of motor cortex

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11
Q

Give some examples of anatomical landmarks of some dermatomes.

A

T5 = level of the nipples

T10 = umbilicus

T12 = inguinal ligament

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12
Q

Outline the arterial supply of the spinal cord.

A

Anterior spinal artery:

  • supplies the anterior 2/3 of the spinal cord
  • supplies spinothalamic tracts and lateral corticospinal tracts

Posterior spinal artery:

  • supplies posterior 1/3 of spinal cord
  • supplies dorsal columns

Intercostal artery —> spinal artery & muscular branch of intercostal artery

Arteries connecting the aorta and the spinal cord arteries:

  • cervical radicular artery
  • thoracic radicular artery
  • radicularis magnus (artery of Adamkiewicz; usually on the left, usually from ~T8-L1)
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13
Q

What is anterior cord syndrome? What is the aetiology? What are the signs and symptoms which result?

A

Ischaemic damage to anterior 2/3 of spinal cord due to occlusion of the anterior spinal artery

Causes:

  • atherosclerosis
  • aortic aneurysm/thrombosis/dissection (+ surgery to treat these) due to damage to artery of Adamkiewicz
  • external compression e.g. herniated disc, neoplasm, posterior osteophyte, kyphoscoliosis
  • trauma to aorta (direct stab injuries)
  • vasculitis (giant cell arteritis)
  • sickle cell anaemia
  • hypotension
  • cardiac emboli (TIA)

Presentation:

  • acute ( complete paralysis below level of lesion on both sides
  • lateral spinothalamic tracts damaged —> loss of pain and temperature sensation below level of lesion on both sides
  • autonomic dysfunction —> postural hypotension
  • bladder/bowel/sexual dysfunction (depending on level of lesion)

note: dorsal columns spared —> 2-point discrimination, proprioception, and vibration sense intact

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14
Q

What are the signs and symptoms associated with damage to the sensory cortex of the parietal lobe?

A

Loss of graphaesthesia (ability to recognise writing on the skin by touch)

Astereognosis = failure to recognise objects by palpation in the absence of visual or auditory information
e.g. know what a pen is but do not recognise a pen placed in their hands

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15
Q

What systems can be damaged to cause nystagmus?

A

Cerebellum

Brainstem

Vestibulocochlear

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16
Q

What is dysphonia? Give some examples of causes.

A

Hoarse/whispered speech

Causes:

  • vocal cords fail to generate sound e.g. laryngitis, recurrent laryngeal nerve palsy
  • higher level problem in vocal cord operation (dystonia)
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17
Q

What is dysarthria? Give some examples of causes.

A

Defect in delivery of speech causing poor articulation/slurring of speech

Causes:
- myopathic = problem with muscles of speech —> indistinct, poor articulation of speech (+ weakness of face, tongue, and neck)

  • myasthenic = problem with motor end plate —> indistinct speech with fatigue and dysphonia with fluctuating severity (+ ptosis, diplopia, face and neck weakness)
  • bulbar = problem in brainstem —> indistinct, slurred, nasal speech (+ dysphagia, diplopia, ataxia)
  • scanning/explosive = problem in cerebellum —> slurred speech with impaired timing and cadence (monotonous, loss of modulation, “sing-song”) (+ ataxia, tremor, nystagmus)
  • spastic/pseudo-bulbar = problem in pyramidal tracts —> indistinct, breathy, mumbling speech (+ poor rapid tongue movements, hyperreflexia, jaw jerk)
  • Parkinsonian = problem in basal ganglia —> indistinct, stammering, quiet speech (+ resting tremor, slow shuffling gait, rigidity)
  • dystonic = problem in basal ganglia —> strained, slow, high-pitched speech (+ dystonia, athetosis)
18
Q

What is athetosis?

A

Slow, involuntary, convoluted, writhing movements of fingers, hands, toes, feet, etc.

Occurs in cerebral palsy

19
Q

What is dysphasia? Give some examples of causes.

A

Defect in language content of speech due to problem in cerebral cortex causing inability to produce correct word (anomia = no word/wrong word/nonsense reply)

Causes:
Lesion in Wernicke’s area (posterior temporal/parietal lobe)
- fluent dysphasia = speaks nonsense, normal or increased no. of words produced, usually unaware of this
- difficulty comprehending speech (therefore have difficulty following instructions)

Lesion in Broca’s area (frontal lobe of dominant hemisphere - usually the left)

  • non-fluent dysphasia = difficulty producing sentences due to grammar, halted speech requiring great effort
  • usually comprehend speech (can follow instructions)
20
Q

What is dysmetria?

A

Lack of coordination of movement characterised by an inability to judge distance and correct for it during movement, causing past-pointing

note: worsens when trying to be more accurate/closer to the finger in the finger-nose test (intention tremor)

21
Q

What is the purpose of Romberg’s test?

A

Distinguishes between sensory ataxia and cerebellar ataxia

Sensory ataxia = proprioceptive defect compromised for by vision (therefore loss of balance when eyes are closed - positive Romberg’s sign)

Cerebellar ataxia = integration defect not compromised for by vision (therefore no worse when eyes are closed - negative Romberg’s test)

22
Q

What part of the spinal cord is affected in motor neurone disease?

A

Anterior horn cells

23
Q

Give some differential diagnoses for anterior cord syndrome.

A

Mass lesion e.g.

  • tumour
  • abscess
  • granuloma
  • haematoma
  • disc herniation

Intraspinal haemorrhage

Acute inflammatory demyelinating polyneuropathy e.g. Guillain-Barré

Demyelination, transverse myelitis

Sarcoidosis

TB, syphilis

24
Q

What is the management for anterior cord syndrome?

A

Treat cause

Manage vascular risk factors

Rehabilitation

25
Q

What is an acute intracranial event? How may it present?

A

Includes stroke, head trauma, etc.

S&S:

  • loss of sensory/motor function
  • change in level of consciousness
  • collapse
  • abnormal behaviour (information from relatives helpful)
  • headache
  • “funny turn” (non-specific)
26
Q

Describe some of the causes of acute intracranial events and their respective pathologies.

A

Lack of blood:

  • blockage in vessels —> ischaemic stroke
  • systemic hypotension (reason for agitation in shock)
  • increased intracranial pressure —> blood cannot enter cerebral vessels

Lack of glucose:

  • systemic hypoglycaemia —> unsteady, slurred speech, aggressive (differentiate from alcohol intoxication)
  • impaired cerebral circulation —> glucose cannot reach brain

Lack of oxygen:

  • airway problem
  • breathing problem
  • carbon monoxide poisoning

Fitting (convulsion):

  • reticular activating system lost
  • disorganised activity (global or focal)
  • –> increased brain metabolic requirement (active brain cells in seizure and motor movements increase demand, reduced resp. function means less glucose and oxygen is delivered)

Head injury:

  • reticular activating system disturbed —> amnesia, loss of consciousness (degree of disturbance depends on force of injury)
  • axons sheared by traction during deceleration
  • cell bodies damaged by bony prominences of skull

Increased intra-cranial pressure:

  • change in behaviour
  • drop in level of consciousness
  • neurological localising signs
  • change in pupil reaction
  • change in BP, pulse, and breathing (alternating between pauses and rapid breathing)
27
Q

Define a contusion.

A

Bruising (of the brain)

Small bleeds surrounded by oedema

28
Q

What is the mechanism of axonal shearing in head injury?

A

Coup and contrecoup injuries cause axons in different areas of the brain to be alternately stretched and compressed —> shearing —> death of neurone

29
Q

Give some examples of causes of raised intracranial pressure.

A

Brain swelling e.g. encephalitis

Meningeal swelling e.g. meningitis

Space-occupying lesion e.g. extradural haemorrhage, primary cancer, metastasis, abscess

CSF blockage e.g. subarachnoid haemorrhage, benign intracranial hypertension —> hydrocephalus

30
Q

What are the primary and secondary insults that result from acute intracranial events?

A

PRIMARY

  • haematoma
  • contusions
  • haemorrhage
  • diffuse axonal injury

SECONDARY

  • hypoxia
  • hypoperfusion
  • oedema
  • raised intracranial pressure

+ brain injuries disrupt tight junctions —> increased permeability of blood-brain barrier

+ microvessels in the brain can be damaged by clots, but antiplatelets cannot be given (catastrophic haemorrhage)

+ injury —> oxidative stress —> release of inflammatory mediators released

+ possible change in expression of ion channels

+ cerebral oedema results from cytotoxic injury (movement of ions and water) and vasogenic injury (disruption of blood vessels)

31
Q

What is the Monro-Kellie hypothesis?

A

Skull is a rigid box of fixed volume, containing three components (blood, brain, CSF) which have varying abilities to alter their volume to maintain constant pressure

32
Q

How does the brain attempt to compensate for increased intracranial pressure?

A

Venous blood loss

CSF loss

33
Q

How is the cerebral perfusion pressure calculated?

A

Mean arterial pressure - intracranial pressure

34
Q

What is the approximate metabolic demand of the brain at rest?

A

50ml/100g of brain/min

20% of total oxygen

35
Q

Why is the cerebral perfusion pressure decreased in hypoxia and hypercapnia?

A

Vasodilatation (attempt to remove CO2 and provide more oxygen to brain) —> oedema —> raised intracranial pressure —> reduced cerebral perfusion pressure

note: can give drugs to induce coma to reduce the oxygen demand of the brain (“hibernation”)

36
Q

Describe the indications of anaesthetic drugs in acute intracranial event.

A

Propofol = induction of anaesthesia

OR Thiopentone = reliable induction of anaesthesia (reliable onset; large volume of redistribution - short duration advisable)

  • reduce cerebral metabolic requirement for oxygen
  • reduce airway reflexes to allow intubation
    note: dose-dependent hypotension (reduced brain perfusion

Opioids

  • pain relief to reduce stress response (even whilst unconscious) and prevent raised intracranial pressure
  • reduce cough (even whilst unconscious) to prevent raised intracranial pressure and enable intubation
    note: can exacerbate hypotension

Ketamine

  • dissociative
  • haemodynamically stable
  • no loss of airway reflexes (cannot intubate)
    note: cause hallucinations/terrors (give benzodiazepines to reduce emergence phenomenon)

Neuromuscular blocking agents
- paralysis to enable intubation

Mannitol/hypertonic saline

  • buy time for surgery by reducing oedema via osmotic diuresis
    note: can also worsen oedema by crossing a leaky blood-brain barrier

Vasopressors e.g. noradrenaline

  • can help adjust BP when other hypotensive agents are given
    note: requires a large line to administer (if given into IJV would impair venous drainage and change the cerebral perfusion pressure) and invasive BP monitoring
37
Q

What is emergence phenomenon?

A

Delirium on recovery from anaesthesia

38
Q

What are some important ITU measurements and considerations?

A

Make sure tubes are unobstructed (tape to face)

Keep patients at 30 degrees (optimise cerebral perfusion pressure)

Measurements:

  • EEG (?seizures)
  • Bispectral index (BIS) = monitors concentration of IV anaesthetics (equivalent of MAC)
  • physiological markers of wakefulness e.g. groaning, twitching, tears (indicates coughing), colour, BP, pulse
39
Q

How can intracranial pressure be measured?

A

Probe (“bolt”)

  • intraventricular (gold standard)
  • subdural (easy)
  • subarachnoid
40
Q

How does the intracranial pressure change in a patient being transported by ambulance?

A

Acceleration —> fluid moves into feet —> reduced intracranial pressure

Deceleration —> fluid moves into head —> increased intracranial pressure

41
Q

Define dyspraxia.

A

Difficulty in putting complex tasks together

42
Q

What sensation is lost first in peripheral neuropathy?

A

Vibration lost first (unnoticed)

Then the longest nerves are affected —> soft touch and deep touch is lost in glove and stocking distribution

Integrative (10 decks)

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