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3ayeeeee > Neuro > Flashcards

Neuro Flashcards

1
Q

What happens with upper motor neuron lesions ?

A
  • Everything goes up !
  • Spasticity
  • Brisk reflexes
  • Plantars are upturned on stimulation
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2
Q

What happens for lower motor neuron lesions ?

A
  • Everything goes down
  • Muscle tone reduced – flaccid
  • Muscle wasting
  • Fasciculations = visible spontaneous contraction of motor units
  • Reflexes depressed or absent
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3
Q

Where are the lower motor neurons located ?

A
  • Anterior horns of the spinal cord and in cranial nerve nuclei in the brain stem
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4
Q

What can ataxia result from ?

A
  • Disorder of the cerebellum and associated pathways
  • Loss of proprioceptive sensory unput in peripheral nerve disorders and in spinal cord lesions affecting the posterior column (sensory ataxia)
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5
Q

Signs of cerebellar disease

A
  • DANISH
  • Dysdiadochokinesis
  • Ataxia
  • Nystagmus
  • Intention tremor
  • Scanning/staccato or slurred speech (dysarthria)
  • Hypotonia
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6
Q

What is Bell’s Palsy ?

A
  • An acute and unliteral facial nerve palsy
  • Unilateral involvement of all facial zones equally that fully evolve within 72 hours
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7
Q

What percentage of patients get full recovery after a Bell’s palsy and how long could it take ?

A
  • 70% of untreated cases
  • Recovery occurs within 4-6 months
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8
Q

Epidemiology of Bell’s Palsy ?

A
  • Equally common in males and females
  • Risk increase x3 with pregnancy and x5 with DM
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9
Q

Clinical features of Bell’s Palsy ?

A
  • Abrupt onset with complete unilateral facial weakness at 24-72 hours
  • Numbness or pain around the ear
  • Decreased taste
  • Hypersensitivity to sounds
  • Patients will be unable to wrinkle forehead (confirming LMN pathology)
  • Also unilateral mouth sagging, drooling, failure of eye to close (watery or dry)
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10
Q

DDs for Bell’s Palsy (7th nerve palsy)

A
  • Infective: Ramsay Hunt Syndrome Lyme disease, meningitis, TB
  • Brainstem lesion: Stoke, tumour or MS
  • Cerebellopontine angle tumours: acoustic neuroma, meningioma
  • Systemic disease: DM or Guillian-Barre
  • Local disease: Parotid tumour, otitis media
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11
Q

Causes of bilateral facial weakness

A
  • GB
  • Sarcoid
  • Trauma
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12
Q

Tests for Bells Palsy (rule out DDs)

A
  • Rule out other causes
  • Bloods – ESR, glucose – raised borrelia ABs in lyme disease – raised VZV ABs in Ramsay Hunt Syndrome
  • CT/MRI – space occupying lesion, stroke, MS
  • CSF (rarely done) for infections
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13
Q

Management of Bell’s Palsy

A
  • Prednisolone within 72 hours
  • Eye protection – dark glasses, artificial tears if drying, pull lid down by hand and use tape to close eyes at night
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14
Q

What is Ramsay Hunt Syndrome

A
  • Latent varicella zoster virus reactivating in the geniculate ganglion of the 7th cranial nerve
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15
Q

Symptoms of Ramsay Hunt Syndrome ?

A
  • Ipsilateral facial palsy, loss of taste, vertigo, tinnitus, deafness, dry mouth and eyes
  • Painful vesicular rash on the auditory canal +/- on drum, pinna, tongue palate or iris
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16
Q

How is Ramsy Hunt Syndrome diagnosed and treated ?

A
  • Clinically as antiviral treatment is thought to be the most effective within the first 72 hours
  • Aciclovir and prednisolone
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17
Q

What is myelopathy ?

A
  • Spinal cord compression
  • Resulting in UMN signs and specific symptoms depending on where the compression is
  • Not typically painful
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18
Q

Potential causes of myelopathy ?

A
  • Vertebral body tumours – MCC – secondary from lung breast, prostate, myeloma or lymphoma (oncological emergency)
  • Spinal pathology – disc herniation or disc prolapse
  • Rare causes – infection, haematomas or primary tumour e.g. Glioma or neurofibroma
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19
Q

What is disc herniation ?

A
  • When the centre of the disc (nucleus pulposus) has moved out through the annulus (outer part of the disc) resulting in pressure on the nerve root and pain
  • Cause of myelopathy
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20
Q

What is disc prolapse ?

A
  • When the nucleus pulposus moves and presses against the annulus but doesn’t escape
  • Producing a bulge which can compress the spinal cord but less so than a herniation
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21
Q

Symptoms of myelopathy

A
  • Bilateral leg weakness (contralateral spasticity and hyperreflexia)
  • Bladder and sphincter involvement (late signs) – hesitancy, frequency  painless retention
  • Spinal or root pain may precede leg weakness and sensory loss
  • Sensory loss below the level of the lesion
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22
Q

Signs of myelopathy

A
  • Onset may be acute (hours to days) or chronic (weeks to months) depending on the cause
  • LMN signs found at the level and UMN below the level
  • Reflexes are usually reduced initially in acute compression
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23
Q

What is sciatica ?

A
  • Compression of the S1 nerve root
  • Sensory loss/pain in back of the thigh/leg/lateral aspect of the little toe (sciatic nerve distribution)
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24
Q

DDs for myelopathy

A
  • Transverse myelitis
  • MS
  • Cord vasculitis
  • Trauma
  • Dissecting aneurysm
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25
Q

Diagnosis of myelopathy

A
  • Do not delay imaging
  • MRI is gold standard – identifies the site and cause of cord compression
  • Biopsy/surgical exploration may be required to identify the nature of any mass
  • Screening blood tests – FBC, ESR, B12, U&E, syphilis serology, LFT, PSA
  • Chest X-ray if TB or malignancy e.g. primary lung
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26
Q

Treatment for myelopathy

A
  • If malignancy – IV dexamethasone (high dose) reduced inflammation/oedema around malignancy and improves outcome
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27
Q

What is cauda equine syndrome ?

A
  • A medical emergency where the nerve roots of the cauda equina become compressed
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28
Q

What do the nerves of the cauda equina supply ?

A
  • Sensation to the lower limbs, perineum, bladder and rectum
  • Motor innervation to the lower limbs, anal and urethral sphincters
  • Parasympathetic innervation to bladder and rectum
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29
Q

Common cause of cauda equina ?

A
  • Herniation at L4/5 and L5/S1
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30
Q

Aetiology for cauda equina ?

A
  • Herniation at L4/5 and L5/S1
  • Tumour/metastases
  • Trauma
  • Infection Spondylolisthesis
  • Post-op haematoma
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31
Q

Pathophysiology of CE

A
  • Nerve root compression caudal to the termination of the spinal cord at L1/L2 so nerves being compressed are LMN that have already exited the spinal cord
  • Usually large central disc herniations at L4/L5 or L5/S1 levels
  • Generally S1-S5 compression (important for balder function)
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32
Q

Clinical presentation for CE

A
  • Saddle anesthesia
  • Bowel incontinence, bladder retention
  • Reduced sphincter tone
  • Erectile dysfunction
  • Bilateral sciatica
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33
Q

Red Flags in CE and DDs

A
  • Saddle anesthesia
  • Loss of sensation in bladder and rectum
  • Urinary retention or incontinence
  • Bilateral sciatic
  • Bilateral or severe motor weakness in legs
  • Reduced anal tone on PR exam
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34
Q

DDs for CE

A
  • Conus medullaris syndrome
  • Vertebral facture
  • Peripheral neuropathy
  • Mechanical back pain
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35
Q

DD of CE

A
  • MRI to localise lesion
  • Knee flexion (to test L5-S1)
  • Ankle plantar flexion (downwards) to test S1-S2
  • Straight leg raising (to test L5-S1), people with acute disc can barley get leg of bed
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36
Q

Treatment for CE

A
  • Refer to neurosurgeon ASAP to relieve pressure or risk irreversible paralysis/ sensory loss/incontinence
  • Microdiscectomy
  • Epidural steroid injection
  • Surgical spine fixation
  • Spinal fusion
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37
Q

Components of a GCS

A
  • Motor (6)
  • Verbal (5)
  • Eyes (4)
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38
Q

Motor points of a GCS score ?

A
  • Obeying commands
  • Localising to pain
  • Withdrawing to pain
  • Flexor response to pain
  • Extensor response to pain
  • No response to pain
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39
Q

Verbal points of a GCS score ?

A
  • Orientated
  • Confused conversation
  • Inappropriate words
  • Incomprehensible words
  • None
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40
Q

Eye points of a GCS score ?

A
  • Spontaneous
  • In response to speech
  • In response to pain
  • None
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41
Q

What is delirium ?

A
  • An acute confusional state seen commonly in elderly patients
  • Characterised by disturbance of consciousness, perception, sleep-wake cycle, emption and cognition
42
Q

Aetiology of Delirium

A
  • DELIRIUMS
  • Drugs  anti-cholinergic, benzos, anti-convulsant
  • Electrolytes  Uremia, Wernicke’s
  • Lack of drugs  Levodopa, opiates, alcohol
  • Infection
  • Reduced sensory  Deaf, blind
  • Retention  Stool or urine
  • Intracranial issues  Post-itcal or stroke
  • Underhydration or nutrition
  • Myocardia
  • Subdural sleep, surgery or pain
43
Q

Symptoms of delirium

A
  • Inattention
  • Altered consciousness
  • Altered sleep wake cycle
  • Hallucinations and mood changes
  • Hypoactive: apathy, withdrawal and quite
  • Hyperactive: agitation, delusions and disorientation
44
Q

Investigations for delirium

A
  • Cognitive screen – MMSE, MOCA, AMTS, AMT
  • Bloods – FBC CRP U+E, LFT, glucose, TFTs, cultures
  • Septic screen – urine dipstick, MSU, Chest-Xray and blood cultures
45
Q

Medication treatment for extremely agitated delirious patients

A
  • Haloperidol or olanzapine
46
Q

Clinical features of delirium

A
  • Globally impaired cognition, perception and consciousness which develops over hours/days characterised by a marked memory deficit, disordered or disoriented thinking and reversal of the sleep-wake cycle
47
Q

RFs for delirium

A
  • Dementia/previous cognitive impairment
  • Hip fracture
  • Acute illness
  • Psychological agitation e.g. pain
48
Q

What is Guillain-Barre Syndrome ?

A
  • An acute, autoimmune, inflammatory, demyelinating ascending polyneuropathy affecting the peripheral nervous system (Schwann cells) following an URT or GI infection
49
Q

Clinical presentation of Guillain-Barre Syndrome

A
  • Paraesthesia without sensory loss
  • Absence of deep tendon reflexes
  • Increased CSF albumin
50
Q

Peak incidence of Guillain-Barre Syndrome

A
  • 15-35yo and 50-75yo
  • MC acute polyneuropathy
  • More common in males
51
Q

Causes of Guillain-Barre Syndrome

A
  • MCC – Campylobacter jejuni
  • Cytomegalovirus
  • Mycoplasma
  • Zoster
  • HIV
  • EBV
  • In some cases idiopathic
52
Q

Pathophysiology of GBS

A
  • GBS is usually triggered by an infection
  • Organism shared the same or similar antigens as those on the Schwann cells (PNS) which leads to autoantibody mediated nerve cell damage formation via molecular mimicry
  • Autoimmune attack causes demyelination  reduction in peripheral nerve conduction  acute polyneuropathy
53
Q

Clinical presentation Guillain-Barre Syndrome

A
  • 1-3 weeks post infection
  • Symmetrical ascending muscle weakness
  • Proximal muscles are more affected
  • Respiratory muscles and facial muscle affected
  • Pain is common
  • Sensory signs absent
  • Reflexes lost early in illness
  • Autonomic features – Sweating, raised pulse, BP change
  • Progressive phase up to 4 weeks followed by recovery
54
Q

Diagnosis of GBS

A
  • Nerve condition studies
  • Lumbar puncture done at L4 – raised protein but normal CSF count
  • Spirometry
  • Immunoglobulin levels
55
Q

Treatment for GBS

A
  • IV immunoglobulin for 5 days – reduces duration and severity of paralysis
  • Plasma exchange
  • Supportive Management
  • Reduce VTE risk, swallowing, neuropathic pain, depression,
56
Q

How do you treat neuropathic pain ?

A
  • 1st Gabapentin
  • Carbamazepine
  • Tramadol
57
Q

Prognosis for GBS

A
  • Good with 85% making a complete/near recovery
  • 10% are unable to walk alone at 1 year
  • Mortality is 10%
  • Poor outcomes associated with old age, preceding diarrhoea illness, severity, rapid deterioration
58
Q

What is Brown-Seqard Syndrome ?

A
  • Lateral hemisection of the spinal cord
59
Q

What are the presenting features of Brown-Seqard Syndrome ?

A
  • Ipsilateral weakness below the lesion
  • Ipsilateral loss of proprioception and vibration sensation
  • Contralateral loss of pain and temperature sensation
  • E.g. Right sided wound = weakness of the right leg, loss of proprioception and vibration sensation and loss of pain and temperature sensation in the left leg
60
Q

Stroke with quadriplegia and small reactive pupils. History of HTN

A
  • Pontine haemorrhage
61
Q

What is autonomic dysreflexia

A
  • A clinical syndrome that occurs in patients who have a spinal cord injury at or above T6
  • Afferent signals most commonly triggered by faecal impaction or urinary retention cause a sympathetic spinal reflux via thoracolumbar outflow
  • The usual centrally mediated parasympathetic response however is prevented by the cord lesion
  • The result is an unbalanced physiological response, characterised by extreme hypertension, flushing, agitation and sweating above the level of the cord lesion
  • In extreme causes of HTN hemorrhagic stroke can occur
62
Q

A painful 3rd nerve palsy is caused by what until proven otherwise ?

A
  • Posterior communicating artery aneurysm
63
Q

Used to treat oedema around tumours in the CNS ?

A
  • Dexamethasone
64
Q

What is ROSIER used for ?

A
  • Recognition of strokes in the emergency room
  • Used to differentiate between strokes and stroke mimics
65
Q

Tools used in strokes

A
  • ROSIER – stokes in the emergency room
  • ABCD2 – risk of stoke after TIA
  • CHA2DS2-VASc – likelihood of stroke secondary to AF
66
Q

Used to identify patients at risk of pressure sores

A
  • Waterlow score
67
Q

Screening tools for dementia

A
  • 10 point cognitive score (10-CS)
  • 6 item cognitive impairment test (6CIT)
68
Q

What is normal ICP

A
  • 7-15 in adults in a supine position
69
Q

What is cerebral perfusion pressure ?

A
  • Net pressure gradient causing blood flow to the brain
  • CPP = mean arterial pressure
70
Q

What are the causes of raised ICP

A
  • Idiopathic
  • Trauma
  • Infection
  • Tumours
  • Hydrocephalus
71
Q

Features of ICP

A
  • Headaches
  • Vomiting
  • Reduce levels of consciousness
  • Papilloedema
  • Cushing’s triad
72
Q

How is raised ICP investigate

A
  • CT/MRI
  • Invasive ICP monitoring = catheter into the lateral ventricles of the brain to monitor pressure (may also collect and drain small amount of CSF)
73
Q

How is raised ICP managed ?

A
  • Investigate and treat the underlying cause
  • Head elevated at 30 degrees
  • IV mannitol may be used as an osmotic diuretic
  • CSF can be drained or repeated LP
  • Controlled hyperventilation Co2  vasoconstriction
74
Q

How will a 3rd nerve palsy present ?

A
  • Down and out eye
  • Ptosis
  • Pupil may be dilated (surgical 3rd nerve palsy)
75
Q

Causes of a 3rd nerve palsy

A
  • DM
  • Vasculitis e.g. temporal arteritis or SLE
  • Posterior communicating artery aneurysm
  • MS
76
Q

What factors would suggest delirium vs dementia ?

A
  • Acute onset
  • Impairment of consciousness
  • Fluctuation of symptoms: worse at night and periods of normality
  • Abnormal perception e.g. illusions and hallucinations
  • Agitation fear
  • Delusions
77
Q

What factors would suggest depression over dementia ?

A
  • Shorter history and rapid onset
  • Biological symptoms e.g. weight loss and sleep disturbance
  • Patient worried about poor memory
  • Reluctant to take tests: disappointed with results
  • Mini-mental test score: variable
  • Global memory loss (dementia is recent memory loss)
78
Q

Medications for Parkinson’s

A
  • Levodopa nearly always combined with decarboxylase inhibitor e.g. carbidopa
  • Dopamine agonist e.g. bromocriptine
  • MAO-B inhibitor – selegiline
  • Consider Glycopyronium bromide for drooling ]
79
Q

Side effects of Levodopa

A
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
  • Dyskinesia at peak dose
80
Q

SEs of dopamine receptor agonists

A
  • Impulse control disorders
  • Excessive daytime somnolence
  • Hallucinations
  • Nasal congestions
  • Postural hypotension
81
Q

Medications for dementia

A
  • The three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine)
  • Donepezil – contraindicated with bradycardia – adverse effects include insomnia
82
Q

Hereditary for Essential tremor

A
  • Autosomal dominant
83
Q

Medication of essential tremor

A
  • Propranolol is 1st line
  • Primidone is sometimes used
84
Q

Typical Presentation of Vascular Dementia

A
  • Stepwise deterioration of cognitive function
  • Focal neurological abnormalities e.g. visual disturbances
  • Attention and concentration difficulty
  • Seizures
  • Memory, gait, speech and emotional disturbance
85
Q

NINDS-AIREN criteria of vascular dementia

A
  • The presence of cognitive decline that interferes with activities of daily living not due to effects of the cerebrovascular event
  • Cerebrovascular disease
  • A relationship between the above 2 disorders inferred by
  • The onset of the dementia within 3 months following a recognised stroke
  • An abrupt deterioration in cognitive function
  • Fluctuating, stepwise progression of cognitive deficits
86
Q

Psychological Therapies Dementia

A
  • Cognitive stimulation programs e.g. music and art therapy or animal assisted therapy
  • Managing challenging behaviour e.g. address pain, avoid overcrowding and have clear communication
87
Q

Features suggesting MND

A
  • Asymmetric limb weakness (MC presentation)
  • Mixture of lower and upper motor neuron signs
  • Wasting of the small hand muscles/tibialis anterior is common
  • Fasciculations
  • Absence of sensory signs/symptoms
  • Doesn’t affect the external ocular muscles
  • No cerebellar signs
88
Q

Most common type of MND

A
  • Amyotrophic lateral sclerosis
89
Q

Medications for MND

A
  • Riluzole
  • Baclofen for muscle spasticity
  • Non-invasive ventilation at night
  • PEG
90
Q

McDonald criteria for MS an individual must have:

A
  • Evidence of CNS damage that is disseminating in space, or appearing in multiple regions of the nervous system.
  • Evidence of damage that is disseminating in time, or occurring at different points in time.
91
Q

Most common presentation in MS

A
  • Optic neuritis
  • Demyelination of the of the optic nerve presenting with unilateral reduced vision developing over hours to days
92
Q

Key features of optic neuritis

A
  • Central scotoma (an enlarged central blind spot)
  • Pain
  • Impaired colour vision
  • Relative afferent pupillary defect – where the pupil in the affected eye constricts more when shinning light in the contralateral eye than when shinning in the affected eye
93
Q

MS focal weakness symptoms

A
  • Incontinence
  • Horner syndrome
  • Facial nerve palsy
  • Limb paralysis
94
Q

MS focal sensory symptoms

A
  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia
  • Lhermitte’s sign
95
Q

What is Lhermitte’s sign

A
  • An electric shock sensation that travels down the spine into the limbs when flexing the neck indicating disease in the cervical spinal cord in the dorsal column
  • It is caused by stretching the demyelinated dorsal column
96
Q

What is Hoffman’s sign

A
  • An involuntary flexion movement of the thumb and or the index finger when the examiner flicks the fingernail of the middle finger down
97
Q

What is Romberg’s test ?

A
  • Lose balance when standing with their eyes closed
98
Q

What are the types of MS ?

A
  • Clinically isolated syndrome
  • Relapsing remitting
  • Secondary progressive
  • Primary progressive
99
Q

What is Gowers sign

A
  • To stand up a child will get onto their hands and knees and then push their hips up and backwards like the ‘’downward dog’’ yoga pose
  • They then shift their weight backwards and transfer their hands to their knees
  • Whilst keeping their legs mostly straight they walk with their hands up their legs to get their upper body to erect
100
Q

Management of Muscular Dystrophy

A
  • Oral steroids slow progression
  • Creatine supplementation can give slight improvement of muscle strength

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