Nervous System Disorders Flashcards
What part of the nervous system is affected in poylradiculoneuropathies?
Multiple nerve roots
What is the classic gait which occurs in hemiparesis due to stroke?
Circumductive
Arms flexed, finger flexed, legs extended
Contrast spasticity and rigidity.
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)
What is clonus? How is it detected? How many beats is considered abnormal when testing ankle clonus?
Sustained clonic (to and fro) contractions across a joint
Stretching of gastrocnemius by dorsiflexing the foot
Over 2 beats is abnormal
What is Babinski’s sign? Why is it abnormal?
Extensor plantar response + fanning of the toes
This pushes the foot towards the pain stimulus instead of away
What is Hoffman’s sign?
Flick finger (hyperextension)
Normal = flexing of finger only
Abnormal = flexing spreads to other fingers/thumb
note: same principle applies when testing tendon reflexes
What is the pathophysiology of fasciculations?
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)
What muscle wasting occurs in ulnar nerve damage or TI nerve root damage?
Wasting of dorsal interossei muscles
Causes “guttering” (loss of first dorsal interossus - between thumb and index finger)
Describe the patterns of weakness and sensory loss in different LMN lesions.
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)
Describe the patterns of weakness and loss of sensation in different UMN lesions.
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
Give some examples of anatomical landmarks of some dermatomes.
T5 = level of the nipples
T10 = umbilicus
T12 = inguinal ligament
Outline the arterial supply of the spinal cord.
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)
What is anterior cord syndrome? What is the aetiology? What are the signs and symptoms which result?
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
What are the signs and symptoms associated with damage to the sensory cortex of the parietal lobe?
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
What systems can be damaged to cause nystagmus?
Cerebellum
Brainstem
Vestibulocochlear
What is dysphonia? Give some examples of causes.
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)
What is dysarthria? Give some examples of causes.
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)
What is athetosis?
Slow, involuntary, convoluted, writhing movements of fingers, hands, toes, feet, etc.
Occurs in cerebral palsy
What is dysphasia? Give some examples of causes.
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)
What is dysmetria?
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)
What is the purpose of Romberg’s test?
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)
What part of the spinal cord is affected in motor neurone disease?
Anterior horn cells
Give some differential diagnoses for anterior cord syndrome.
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
What is the management for anterior cord syndrome?
Treat cause
Manage vascular risk factors
Rehabilitation
What is an acute intracranial event? How may it present?
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)
Describe some of the causes of acute intracranial events and their respective pathologies.
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)
Define a contusion.
Bruising (of the brain)
Small bleeds surrounded by oedema
What is the mechanism of axonal shearing in head injury?
Coup and contrecoup injuries cause axons in different areas of the brain to be alternately stretched and compressed —> shearing —> death of neurone
Give some examples of causes of raised intracranial pressure.
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
What are the primary and secondary insults that result from acute intracranial events?
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)
What is the Monro-Kellie hypothesis?
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
How does the brain attempt to compensate for increased intracranial pressure?
Venous blood loss
CSF loss
How is the cerebral perfusion pressure calculated?
Mean arterial pressure - intracranial pressure
What is the approximate metabolic demand of the brain at rest?
50ml/100g of brain/min
20% of total oxygen
Why is the cerebral perfusion pressure decreased in hypoxia and hypercapnia?
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”)
Describe the indications of anaesthetic drugs in acute intracranial event.
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
What is emergence phenomenon?
Delirium on recovery from anaesthesia
What are some important ITU measurements and considerations?
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
How can intracranial pressure be measured?
Probe (“bolt”)
- intraventricular (gold standard)
- subdural (easy)
- subarachnoid
How does the intracranial pressure change in a patient being transported by ambulance?
Acceleration —> fluid moves into feet —> reduced intracranial pressure
Deceleration —> fluid moves into head —> increased intracranial pressure
Define dyspraxia.
Difficulty in putting complex tasks together
What sensation is lost first in peripheral neuropathy?
Vibration lost first (unnoticed)
Then the longest nerves are affected —> soft touch and deep touch is lost in glove and stocking distribution
