Neurological Disorders Flashcards
Contrast the signs in patients with unilateral cerebellar damage and patients with damage to the vermis of the cerebellum.
Unilateral cerebellar damage = patient sways and tends to fall towards the SAME SIDE as the lesion
Damage to vermis of cerebellum = patient loses balance and falls BACKWARDS
What can mimic cerebellar dysfunction/cause temporary cerebellar dysfunction?
Alcohol intoxication
Describe the causes of vitamin B12 deficiency, and what effect this can have on the nervous system.
Aetiology:
- lack of intrinsic factor (congenital or due to gastrectomy) —> pernicious anaemia
- bacterial overgrowth competing for vitamin B12 (blind-loop syndrome)
- lack of absorption (ileal resection or Crohn’s disease)
- malnutrition
Can cause subacute combined degeneration of the cord (myelin degradation of the dorsal and lateral columns)
- spasticity, reduced coordination, and impaired sensation in the lower limbs
- optic atrophy
- cerebral changes —> psychiatric disease
Describe what effects pyridoxine/vitamin B6 deficiency can have on the nervous system.
Reversible ataxia & progressive sensory neuropathy
Due to degeneration of dorsal columns (loss of light touch, 2-point discrimination, and conscious proprioception)
Describe what effects syphilis (tertiary?) can have on the nervous system.
Dorsal column loss (tabes dorsalis)
S&S:
- dementia
- paraesthesia (“lightning”)
- weakness
- hyporeflexia
- locomotor ataxia
- degeneration of joints
- positive Romberg’s test
- episodes of intense pain & disturbed sensation
- urinary incontinence
- deafness
- visual impairment
- Argyll-Robertson pupil (loss of light reflex - consensual???)
What is Friedreich’s ataxia?
Congenital degeneration of the spinal cord
S&S:
- progressive ataxia of limbs & gait (degeneration of dorsal root ganglia)
- dysarthria, dysphagia, visual & hearing loss (degeneration of cranial nerves)
- extensor plantar responses (positive Babinski reflex?)
- areflexia
- pyramidal weakness in lower limbs
- loss of joint position & vibration in lower limbs
note: vitamin E deficiency can present the same way but is treatable and reversible
Describe which areas of the spinal cord can be affected by different neurological diseases.
Dorsal columns:
- subacute combined degeneration (vitamin B12 deficiency)
- Friedreich’s ataxia
- tabes dorsalis (syphilis)
Ventral horn cells:
- motor neurone disease
- spinomuscular atrophy
Ventral corticospinal tract:
- motor neurone disease
Spinocerebellar tract:
- Friedreich’s ataxia
Lateral corticospinal tract:
- motor neurone disease
- subacute combined degeneration (vitamin B12 deficiency)
- Friedreich’s ataxia
What is syringomyelia?
Formation of a longitudinal cavity within the spinal cord (syrinx)
Congenital or acquired (via repeated trauma over ~15yrs-20yrs to the cervical cord —> scarring —> cyst formation)
Can expand ventrally to compress motor nerve cells & the spinothalamic tract —> weakness and wasting of the muscles in hands & loss of awareness of pain and temp.
Can cause effective transection of the spinal cord
Give some examples of UMN signs.
Remove inhibitory effect
- spastic paralysis —> loss of voluntary control of muscles (but muscles are still innervated and contract reflexively, so there is no muscle wasting)
- hypertonia (spasticity) —> stiff joints (arms flexed and legs extended)
- hypereflexia (flexor reflexes predominate in upper limbs, extensor reflexes predominate in lower limbs; particularly evident when present on one side only)
- clonus
- Babinski’s sign
- choreiform movements
- facial paralysis will be forehead-sparing (UMNs to upper face project to facial nuclei bilaterally) and contralateral
- pronator drift
- loss of abdominal reflexes (inc. cremasteric reflex)
- sensory deficits involve quadrants or halves of the body
Define spastic paralysis.
Weakness of limb associated with increased reflex activity
—> resistance to passive movement (agonist and antagonist muscles contract simultaneously? CHECK)
—> normal body posture and gait affected
What is lead pipe rigidity? Give an example of disorder it occurs in.
Hypertonia causing sustained resistance to passive movement throughout whole range of motion (no fluctuations)
Parkinson’s disease
What is cogwheel rigidity? Give an example of a disease it occurs in.
Lead pipe rigidity + resting tremor = jerky resistance to passive movement as muscles tense and relax
Parkinson’s disease
Define clonus. What is the pathophysiology? CHECK!!!
Rhythmical contraction of a muscle in response to a suddenly applied and then sustained stretch stimulus caused by an exaggerated stretch reflex
Due to a loss of desc. inhibition (UMN lesion) —> polysynaptic reflexes are visible (successive contractions after the initial reflex)
Abnormal no. of beats = 2+???
What is Babinski’s sign?
CHECK
Extension/fanning of toes in response to drawing a blunt, pointed object along the lateral sole and across the metatarsals (in an ADULT - normal response is curling inwards of the foot)
POSITIVE OR NEGATIVE?
Define choreiform movements. Give an example of a disorder which has this as a feature.
Brief semi-directed, irregular movements that are not repetitive or rhythmic, but appear to flow from one muscle to the next
Involuntary spasmodic movements of the limb and face
Hyperkinetic movement disorder
Movement is sudden but the resulting posture may be prolonged for a few seconds
e.g. Huntington’s chorea
Give some examples of LMN signs.
- flaccid muscle weakness or paralysis (total transection)
- hypotonia —> atonia (depends on no. of motor neurones affected)
- denervation muscle atrophy
- –> muscle wasting (reduced release of trophic factors at NMJ) —> contractures (muscle replaced by fibrous tissue)
- –> fasciculations (ACUTE) —> no fasciculations (CHRONIC)
- hyporeflexia
- associated sensory deficits likely to have a peripheral nerve pattern
Define flaccid muscle weakness.
Absence of muscle tone in one or both limbs and absent tendon reflexes
Define fasciculations.
Brief spontaneous contraction of a few muscle fibres, seen as a flicker of movement under the skin (ACUTE PHASE)
Explain the pathophysiology of denervation muscle atrophy.
Reduced release of trophic factors at NMJ
- –> fasciculations (ACUTE)
- increased expression of nAChRs to compensate for reduced firing from nerve
- low threshold; so ACh-similar molecules also stimulate (inc. diffuse ACh in the blood supplying the muscles)
- –> no fasciculations (CHRONIC)
- muscle death has occurred
What are some signs of cerebellar dysfunction?
DANISH
Dysmetria/dysdiadochokinesia Ataxia Nystagmus Intention tremor Scanning/slurred speech Hypotonia/hyporeflexia
note: no muscle atrophy/weakness (desc. pathways intact)
note: cannot learn new movements (cerebrocerebellum required to automate new movements)
What are the features of cerebellar ataxia?
COORDINATION:
- clumsiness of voluntary movements
- wide-based “rolling” gait (lurching, reeling)
- maintaining balance difficult due to impaired muscle coordination timing (hypotonia)
- dysmetria (past-pointing)
- dysdiadochokinesis
Nystagmus common
Dysarthria = scanning speech (slow, monotonous)
Intention tremor (movements decomposed into a succession of separate movements instead of one smooth action)
Define dysmetria. What part of the brain is damaged?
“Past-pointing”
Pointing past finger in finger-nose test due to impaired muscle coordination timing —> miss target/large scale error correction required
Contrast with intention tremor
Cerebellum damaged
Define dysarthria. What part of the brain is damaged?
“Scanning speech”
Monotone speech due to impaired movement planning of muscles of face, mouth, and tongue
Cerebellum damaged
Why do cerebellar disorders cause hypotonia and hyporeflexia?
Cerebellum involved in setting muscle tone
What is true writer’s cramp?
Antagonist muscles co-activated —> fine precision movements impaired —> hand locks up
Define dysdiadochokinesia. What part of the brain is damaged?
Abnormal agonist/antagonist muscle coordination —> clumsiness performing rapidly alternating movements
Cerebellum = matches motor output with motor intention and corrects errors (loss of function —> errors not corrected and get worse as action is repeated)
What is an intention tremor? What part of the brain is damaged?
When approaching target in finger-nose test, there is a tremor (increased tremor the closer to the target)
Contrast with resting tremor
Cerebellum = movements decomposed into a succession of movements instead of one smooth action
Give some examples of causes of cerebellar dysfunction.
Tumours
Cerebrovascular disease e.g. stroke
Alcohol (cerebellar atrophy)
Genetic e.g. Friedreich’s ataxia (degeneration of pathways in cerebellum)
What can basal ganglia dysfunction cause?
HYPOkinetic disorders e.g. Parkinson’s disease
HYPERkinetic disorders e.g. Huntington’s disease
Outline the pathophysiology of Parkinson’s disease.
Progressive degeneration of dopaminergic neurones (pigmented) of the pars compacta of the substantia nigra, locus ceruleus, and other brainstem nuclei (50%+ loss —> symptomatic)
Reduced inhibition in neostriatum —> loss of inhibition in neostriatum —> increased ACh production and increased excitation —> chain of abnormal signalling —> impaired mobility
DIRECT PATHWAY:
—> reduced activation of D1 receptors of striatum —> reduced inhibition of globus pallidus interna and pars reticulata of substantia nigra —> increased inhibition of thalamus —> reduced stimulation of striatum and cerebral cortex —> bradykinesia
INDIRECT PATHWAY:
—> reduced inhibition of D2 receptors of striatum —> increased inhibition of globus pallidus externa —> reduced inhibition if subthalamic nucleus —> increased stimulation of globus pallidus interna and substantia nigra
Surviving neurones contain Lewy bodies (round eosinophilic inclusions containing alpha-synuclein) —> becomes widespread —–> diffuse Lewy body disease/dementia
What are the signs and symptoms of Parkinson’s disease?
Triad:
- slow resting tremor (begins in hands - “pill-rolling tremor”); reduced by purposeful movements (basal ganglia involved in planning of movements; so tremor improves once movement begins)
- hypertonia —> lead pipe rigidity
- bradykinesia/akinesia
- postural instability (late change)
- mood changes
- pain
- cognitive change
- sleep disorder
- sweating
- mask-like face (eyes wide open, infrequent blinking)
Lead pipe rigidity + resting tremor = cog-wheel rigidity
Parkinsonian gait
- slow, shuffling gait (marche a petit pas)
- difficult to stop movement (festination)
- slow pedestal turning (unsteady when changing direction)
- difficult to get up from a chair and start walking
- stooped shoulders (flexed posture)
- reduced arm swing
- improved using visual aids e.g. lines on the floor (cerebellum used more)
note: coordination is preserved (bradykinesia may be confused with lack of coordination)
note: usually presents unilaterally initially but becomes bilateral gradually e.g. tremor presents unilaterally and then becomes generalised over months-years (basal ganglia affect the corticospinal and rubrospinal tracts, which decussate —> contralateral side affected initially)
What is Brown-Séquard syndrome? CHECK!!!
Hemisection of the spinal cord causing sensory dissociation causing sensory loss & flaccid weakness in the areas of the body supplied by the damaged segment
Aetiology:
- idiopathic spinal cord herniation
- trauma
- spinal cord mass
- MS
- degenerative e.g. disc herniation
- cystic disease
- haemorrhage/ischaemia
- infection
S&S:
- loss of pain & temp. below the lesion on the CONTRALATERAL side (due to loss of spinothalamic tract - decussates at the approximate level of the lesion)
- spastic paralysis below the lesion & positive Babinski sign on the CONTRALATERAL side (due to loss of corticospinal tract)
- absent position sense, vibration, 2-point discrimination, & light touch at the level of the lesion (CHECK!!!!!) on the IPSILATERAL side (due to of dorsal column - decussates in the medulla)
- pyramidal tract weakness at the level of the lesion (CHECK!!!) on the IPSILATERAL side (due to loss of corticospinal tract)
Dependent on level of lesion:
- sphincter disturbances (nerve roots????)
- sympathetic fibres in neck damaged —> ipsilateral Horner’s syndrome
What is the prognosis of Parkinson’s disease?
15yr follow-up
- 94% dyskinesia
- 81% falls
- 84% cognitive decline (50% hallucinations)
- 80% drowsiness
- 50% dysphagia
- 27% dysarthria
How is Parkinson’s disease diagnosed?
Clinical features
Exclude other causes of Parkinsonism
Response to treatment
Structural neuroimaging is normal
Functional neuroimaging e.g. PET
What are the pharmacological treatments of Parkinson’s disease?
L-dopa/levodopa
note: add peripheral DOPA decarboxylase inhibitor to allow majority to reach the brain
Dopamine receptor agonists e.g. bromocriptine, ropinirole
MAO-B inhibitors e.g. selegiline
- enhance dopamine action by preventing breakdown by MAO-B
COMT inhibitors e.g. entacapone
- reduces peripheral breakdown of L-DOPA
- reduces wearing off L-DOPA (prolongs motor response)
Anticholinergics e.g. procyclidine
- ?antagonistic effect to dopamine
- treats tremor
- ADRs = confusion, drowsiness, usual anticholinergic effects
Amantadine
- ?increased dopamine release
- ?ACh NMDA inhibition
Describe the pharmacokinetics, ADRs, and drug-drug interactions associated with levodopa.
Dopamine replacement
PHARMACOKINETICS:
- actively transported across blood-brain barrier
- converted to dopamine in substantia nigra (9% converted to dopamine in peripheral tissues)
- PO (must add peripheral DOPA decarboxylase inhibitor e.g. co-careldopa, co-beneldopa to increase amount reaching the brain)
- t1/2 = ~2hrs
ADRs:
- limited to functionality of dopaminergic neurones —> treatment failure will eventually result —> akinesia (frozen)
- can cause hyperkinesia (excessive activation of direct pathway and inhibition of indirect pathway; e.g. involuntary movements, dyskinesias, dystonias) alternating with hypokinesia (freezing - stop suddenly; feel as if feet are glued to the floor) (ON/OFF FLUCTUATIONS)
- protein deposits —> Lewy body dementia (fluctuating cognition, visual hallucinations, Parkinsonism)
- wearing off (as L-dopa wears off at end of dose, motor fluctuations occur)
- impulse control behaviours affected (frontal lobe disinhibition) e.g. pathological gambling, hypersexuality
- N&V
- hypotension
- psychosis (schizophrenic-like effects e.g. hallucinations, delusions, paranoia)
- tachycardia
DDIs:
- pyridoxine (vitamin B6) increases peripheral breakdown of L-dopa
- MAO inhibitors —> hypertensive crisis
- anti-psychotics block dopamine receptors —> Parkinsonism
Describe the pharmacokinetics and ADRs associated with dopamine receptor agonists.
e.g. bromocriptine, ropinirole
- de novo or adjuvant
- ergot-derived or non-ergot-derived (reduced ADRs)
ADRs:
- fewer dyskinesia/motor complications than L-DOPA (but less effective)
- impulse control disorders e.g. pathological gambling, hypersexuality, punding, compulsive shopping
- psychiatric symptoms (dose-limiting) e.g. hallucinations, confusion
- sedation e.g. excessive daytime sleepiness
- hypotension
- nausea
- ergot-derived = fibrotic reactions inc. pulmonary fibrosis, retroperitoneal fibrosis, pericardial fibrosis
Define punding. When does it occur?
- intense fascination with repetitive manipulations of technical equipment
- continual handling, examining, and sorting of common objects
- excessive grooming
- hoarding
- fidgeting
- pointless driving/walking
- extended monologues devoid of rational content
Associated with dopamine receptor agonists
What are the surgical treatments of Parkinson’s disease? When is it indicated?
Sterotactic (use of 3D coordinates to locate small targets; minimally invasive) = targets thalamus for tremor and globus pallidus interna for dyskinesias
Deep brain stimulation targets subthalamic nucleus
Useful in people who are dopamine responsive but have significant side-effects to L-DOPA with no psychiatric illness
Give some examples of disorders which are encompassed in Parkinson Plus. What are some red flags for Parkinson Plus?
Drug-induced e.g. dopamine blockers/depleters, anti-psychotics e.g. haloperidol
CO poisoning (mental impairment and residual Parkinsonism as a consequence of hypoxia)
Organic solvent poisoning e.g. carbon disulfide
Progressive supranuclear palsy:
- Parkinsonism
- postural instability with early falls
- rigidity in extension only
- vertical supranuclear gaze palsy
- pseudobulbar palsy
- dementia
Multiple system atrophy:
- Parkinsonism
- ataxia and autonomic symptoms e.g. postural hypotension, urinary incontinence, pyramidal tract dysfunction (Shy-Drager syndrome)
- cerebellar involvement
- disappointing response to L-dopa (due to degeneration of post-synaptic neurones in basal ganglia)
Corticobasal degeneration:
- alien limb phenomenon
- myoclonus
- dementia
Wilson’s disease = screen all under 50yrs with akinetic-rigid syndrome
Red flags:
- symmetrical presentation
- absence of tremor
- poor response to levodopa
- early falls (first yr)
- additional neurological features
Outline the pathophysiology of Huntington’s chorea.
Autosomal dominant
Expansion of trinucleotide repeat
Accumulation of abnormal protein
Affects neostriatum, substantia nigra, hippocampus, cerebral cortex, hypothalamus, thalamus
Symptoms begin in early middle age
What are the signs and symptoms of Huntington’s chorea?
- unsteady gait
- hyperkinetic, jerky, arrhythmic involuntary movements (choreiform)
- behavioural changes e.g. anxiety, depression, blunted affect (reduced display of emotions), aggression, compulsive behaviours
- progressive dementia
Define hemiballismus. What part of the brain is damaged? Give some examples of causes.
Violent involuntary movement usually restricted to one arm and primarily involving the proximal muscles
Basal ganglia
Causes:
- stroke
- haemorrhage
- trauma
Describe the diagnosis and pharmacological management of myasthenia gravis.
Fluctuating, fatiguable weakness of skeletal muscle
- extraocular muscles
- bulbar involvement e.g. dysphagia, dysphonia, dysarthria
- limb weakness
- resp. muscle involvement
DIAGNOSIS: give IV ACh-ase inhibitor and see if muscle weakness improves
Drugs affecting neuromuscular transmission exacerbate e.g.
- aminoglycosides
- beta-blockers
- quinidine, chloroquine
- succinylcholine
- magnesium
- ACE inhibitors
Acute exacerbation —> myasthenic crisis = worsening of muscle weakness resulting in resp. failure that requires intubation and mechanical ventilation
Management = ACh-ase inhibitors
- pyridostigmine = PO; 30min onset, 3-6hr duration
- neostigmine = PO, IV; 4hr duration
- ADRs = SSLUDGE = Salivation, Sweating, Lacrimation, Urinary incontinence, Diarrhoea, GI upset/hypermobility, Emesis
Over-treatment —> cholinergic crisis = over-stimulation at NMJ due to excess ACh —> flaccid paralysis, resp. failure, increased sweating and salivation, miosis
Define: akinesia, apraxia, agnosia, aphasia, areflexia, and ataxia.
AKINESIA = absence or loss of power of voluntary muscles
APRAXIA = loss of purposeful movements despite the preservation of muscle power, sensation, and coordination
AGNOSIA = lack of the perceptual ability to recognise objects
APHASIA = impaired speech communication
AREFLEXIA = absence of reflexes
ATAXIA = loss of muscular coordination
Define: dysphagia, dysarthria, dysphonia, dysdiadochokinesis, dyslexia.
DYSPHAGIA = difficulty swallowing
DYSARTHRIA = slowing/slurring of speech due to loss of coordination of muscles of speech
DYSPHONIA = any disorder in voice production
DYSDIADOCHOKINESIS = difficultly performing repetitive movements
DYSLEXIA = showing a level of reading/writing below expected for measured IQ
Contrast the definitions of hypotonia and hypertonia.
HYPOTONIA = weakened/dampened reflexes
- arise when any component of the muscle stretch reflex is compromised
HYPERTONIA = abnormally high muscle tone
- most commonly seen as spastic paralysis following a stroke damaging UMNs
What is motor neurone disease?
a.k.a amyotrophic lateral sclerosis (ALS), Lou Gehrig’s disease, supranuclear palsy
Damage to lateral (and ventral) part of nervous system causing reduced muscle growth due to denervation atrophy
Lateral = autonomic motor Ventral = somatic motor
- ocular motor nerves & anal sphincter function preserved
- death occurs when respiratory muscles are affected
What areas of the nervous system are damaged in polio myelitis?
Selectively affects motor neurones (in ~0.1%-0.5% of cases)
—> acute flaccid paralysis (spinal, bulbar, or bulbospinal)
note: causes lesion on cell body of alpha-motoneurones (limb muscles and resp. muscles equally vulnerable) —> loss of neuronal innervation —> loss of ability to produce force acutely and chronically (no chance of recovery)
Define: paraplegia, hemiplegia, quadriplegia, ophthalmoplegia.
PARAPLEGIA = paralysis of both of a pair of limbs (usually the legs)
HEMIPLEGIA = paralysis of ipsilateral limbs (arm and leg on the same side)
QUADRIPLEGIA = paralysis affecting all four limbs (also known as tetraplegia)
OPHTHALMOPLEGIA = weakness of extraocular muscles of the eye
Define: paresis, hemiparesis, palsy.
PARESIS = muscular weakness
HEMIPARESIS = weakness affecting one side of the body or face
PALSY = weakness
Contrast spasticity and rigidity.
SPASTICITY = resistance to passive movement of a limb which is maximal at the beginning of movement and gives way as more pressure is applied
RIGIDITY = resistance to passive movement of a limb which persists throughout range
What is a positive Romberg sign? What does it indicate?
Inability to stand with feet together without swaying when eyes are closed.
Patient maintains posture when eyes are open (visual aspect is compensating for loss of balance from vestibular or cerebellar systems)
Lesion in vestibular or cerebellar systems (but cerebellar system damage can be so severe that it causes truncal instability even whilst eyes are open)
What is the classical presentation of a sensory ataxia gait? Give some examples of causes.
- difficulty picking feet up
- stamp feet down
- “stick and stamp”
- exacerbated in the dark (cannot see feet)
Due to impaired sensation in lower limbs
- dorsal columns lost (loss of proprioceptive input) e.g. vit. B12 deficiency —> subacute combined degeneration of the cords
- peripheral nerves lost (loss of sensation) e.g. diabetic peripheral neuropathy
What is the classical presentation of a hemiplegic gait? Give some examples of causes.
Circumductive gait
- unilateral weakness on affected side
- arm flexed, adducted, and internally rotated
- leg extended with plantarflexion
Whilst walking, patient will hold arm to one side and drag affected leg in a semicircle (circumduction) due to footdrop and extensor hypertonia in lower limb
e.g. stroke
What is the classical presentation of a diplegic gait? Give some examples of causes.
- involvement on both sides
- spasticity in lower limbs worse than upper limbs
- extreme tightness of hip adductors —> scissor gait
Patient walks with abnormally narrow base, dragging both legs and scraping toes along the ground.
e.g. cerebral palsy
What is the classical presentation of a neuropathic gait? Give some examples of causes.
“Steppage gait”
Occurs in foot drop - patient attempts to lift leg high enough during walking so that the foot does not drag on the floor
Unilateral e.g. peroneal nerve palsy, L5 radiculopathy
Bilateral e.g. ALS, Charcot-Marie-Tooth, diabetic peripheral neuropathy
What is the classical presentation of a myopathic gait? Give some examples of causes.
“Waddling gait”
- unilateral weakness in gluteus medius and minimus causes pelvis to drop on the contralateral side during walking (Trendelenburg sign)
- bilateral weakness in gluteus medius and minimus causes pelvis to drop on both sides during walking —> waddling gait
e. g. muscular dystrophy
What is the classical presentation of a Parkinsonian gait? Give some examples of causes.
Rigidity + bradykinesia
- stooped
- head and neck forward
- upper limbs in flexion with finger extended
- walks with slow little steps (marche a petits pas)
- difficulty initiating steps
- involuntary acceleration (festination)
e.g. Parkinson’s disease, Parkinson plus, drugs
What is the classical presentation of a choreiform gait? Give some examples of causes.
Irregular, jerky movements in all extremities.
Walking may accentuate baseline movement disorder
e.g. Huntington’s chorea
What is the classical presentation of an ataxic gait? Give some examples of causes.
Cerebellar
- wide based
- clumsy
- staggering
- titubations whilst standing still (truncal instability - vermis of cerebellum affected)
- not be able to walk heel to toe or in a straight line
e.g. alcohol intoxication, cerebellar lesion
What is spinal shock?
Loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes following a spinal cord injury
Initial stage of hyporeflexia following acute lesions
Then there is hyperreflexia
Explain how cervical arthritis can present. How would this be treated?
Spinal nerves emerging from intervertebral foramina of the cervical vertebrae compressed by enlarged apophyseal joints
Presentation depends on nerves affected
e.g. C8/T1 nerves affected: - absent triceps reflex - weak extension and abduction of wrist - weakness of whole hand - paraesthesia of medial side of arm and hand
+ occipital headache
+ neck pain
Treatment:
- cervical collar to limit movement
Describe the presentation and pathophysiology of multiple sclerosis.
Autoimmune destruction of myelin causing formation of scar tissue (sclerosis), resulting in slowed or blocked transmission of impulses.
Genetic and environmental factors e.g. viral infections
S&S:
- visual (optic nerve demyelination) = blindness, hemianopia, optic neuritis
- extraocular = diplopia, symmetrical horizontal jerking nystagmus, lateral rectus palsy
- facial = Bell’s palsy, trigeminal neuralgia, paroxysmal dysarthria
- vestibular = deafness, unsteadiness, positional vertigo, vomiting, ataxia, headache
- cognitive = memory loss
- depression
- spinal tracts = tightness/burning/twisting/pulling sensations or loss of sensation (dorsal columns), loss of pain and temperature sensation (spinothalamic tracts), numbness of perineum and genitalia, altered sphincter function
- transverse myelitis (acute episode of weakness/paralysis of both legs with sensory loss and urinary/faecal incontinence)
- ANS = urgency and frequency urinary incontinence, impotence, loss of thermoregulation
- Horner’s syndrome
- arrhythmias
- acute pulmonary oedema (abnormal vascular responses)
- weight loss
- inappropriate ADH secretion
Relapsing-remitting MS (80%) = periods of remission, but each relapse leaves disability which compound over time (50% develop secondary progressive MS where there are fewer remissions and worsening of symptoms)
Primary progressive MS (10%-15%) = symptoms gradually develop and worsen over time
note: scattered neurological signs are typical of a demyelinating disorder, and the most common explanation is MS
What is the most common cause of lower back pain? How can it be differentiated from other causes?
Soft tissue injury (muscles, ligaments, tendons)
- occurs following back muscle spasms
- no loss of sensation (loss of sensation occurs in sciatica)
- more pain on active movement (use of muscles)
- negative straight leg raise test (sciatic pain between 30-70 degrees indicates sciatica)
- no loss of reflexes (ankle jerk reflex may be lost in sciatica)
