Nervous System Disorders

Question 1

What part of the nervous system is affected in poylradiculoneuropathies?

Answer 1

Multiple nerve roots

Question 2

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

Answer 2

Circumductive

Arms flexed, finger flexed, legs extended

Question 3

Contrast spasticity and rigidity.

Answer 3

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)

Question 4

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

Answer 4

Sustained clonic (to and fro) contractions across a joint

Stretching of gastrocnemius by dorsiflexing the foot

Over 2 beats is abnormal

Question 5

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

Answer 5

Extensor plantar response + fanning of the toes

This pushes the foot towards the pain stimulus instead of away

Question 6

What is Hoffman’s sign?

Answer 6

Flick finger (hyperextension)

Normal = flexing of finger only

Abnormal = flexing spreads to other fingers/thumb

note: same principle applies when testing tendon reflexes

Question 7

What is the pathophysiology of fasciculations?

Answer 7

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)

Question 8

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

Answer 8

Wasting of dorsal interossei muscles

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

Question 9

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

Answer 9

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)

Question 10

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

Answer 10

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

Question 11

Give some examples of anatomical landmarks of some dermatomes.

Answer 11

T5 = level of the nipples

T10 = umbilicus

T12 = inguinal ligament

Question 12

Outline the arterial supply of the spinal cord.

Answer 12

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)

Question 13

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

Answer 13

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

Question 14

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

Answer 14

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

Question 15

What systems can be damaged to cause nystagmus?

Answer 15

Cerebellum

Brainstem

Vestibulocochlear

Question 16

What is dysphonia? Give some examples of causes.

Answer 16

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)

Question 17

What is dysarthria? Give some examples of causes.

Answer 17

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)

Question 18

What is athetosis?

Answer 18

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

Occurs in cerebral palsy

Question 19

What is dysphasia? Give some examples of causes.

Answer 19

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)

Question 20

What is dysmetria?

Answer 20

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)

Question 21

What is the purpose of Romberg’s test?

Answer 21

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)

Question 22

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

Answer 22

Anterior horn cells

Question 23

Give some differential diagnoses for anterior cord syndrome.

Answer 23

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

Question 24

What is the management for anterior cord syndrome?

Answer 24

Treat cause

Manage vascular risk factors

Rehabilitation

Question 25

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

Answer 25

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)

Question 26

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

Answer 26

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)

Question 27

Define a contusion.

Answer 27

Bruising (of the brain) Small bleeds surrounded by oedema

Question 28

What is the mechanism of axonal shearing in head injury?

Answer 28

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

Question 29

Give some examples of causes of raised intracranial pressure.

Answer 29

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

Question 30

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

Answer 30

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)

Question 31

What is the Monro-Kellie hypothesis?

Answer 31

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

Question 32

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

Answer 32

Venous blood loss CSF loss

Question 33

How is the cerebral perfusion pressure calculated?

Answer 33

Mean arterial pressure - intracranial pressure

Question 34

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

Answer 34

50ml/100g of brain/min 20% of total oxygen

Question 35

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

Answer 35

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")

Question 36

Describe the indications of anaesthetic drugs in acute intracranial event.

Answer 36

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

Question 37

What is emergence phenomenon?

Answer 37

Delirium on recovery from anaesthesia

Question 38

What are some important ITU measurements and considerations?

Answer 38

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

Question 39

How can intracranial pressure be measured?

Answer 39

Probe ("bolt") - intraventricular (gold standard) - subdural (easy) - subarachnoid

Question 40

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

Answer 40

Acceleration ---> fluid moves into feet ---> reduced intracranial pressure Deceleration ---> fluid moves into head ---> increased intracranial pressure

Question 41

Define dyspraxia.

Answer 41

Difficulty in putting complex tasks together

Question 42

What sensation is lost first in peripheral neuropathy?

Answer 42

Vibration lost first (unnoticed) Then the longest nerves are affected ---> soft touch and deep touch is lost in glove and stocking distribution