Neuro Flashcards
1
Q
What happens with upper motor neuron lesions ?
A
- Everything goes up !
- Spasticity
- Brisk reflexes
- Plantars are upturned on stimulation
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
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
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)
5
Q
Signs of cerebellar disease
A
- DANISH
- Dysdiadochokinesis
- Ataxia
- Nystagmus
- Intention tremor
- Scanning/staccato or slurred speech (dysarthria)
- Hypotonia
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
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
8
Q
Epidemiology of Bell’s Palsy ?
A
- Equally common in males and females
- Risk increase x3 with pregnancy and x5 with DM
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)
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
11
Q
Causes of bilateral facial weakness
A
- GB
- Sarcoid
- Trauma
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
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
14
Q
What is Ramsay Hunt Syndrome
A
- Latent varicella zoster virus reactivating in the geniculate ganglion of the 7th cranial nerve
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
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
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
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
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
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
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
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
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)
24
Q
DDs for myelopathy
A
- Transverse myelitis
- MS
- Cord vasculitis
- Trauma
- Dissecting aneurysm
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
26
Q
Treatment for myelopathy
A
- If malignancy – IV dexamethasone (high dose) reduced inflammation/oedema around malignancy and improves outcome
27
Q
What is cauda equine syndrome ?
A
- A medical emergency where the nerve roots of the cauda equina become compressed
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
29
Q
Common cause of cauda equina ?
A
- Herniation at L4/5 and L5/S1
30
Q
Aetiology for cauda equina ?
A
- Herniation at L4/5 and L5/S1
- Tumour/metastases
- Trauma
- Infection Spondylolisthesis
- Post-op haematoma
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)
32
Q
Clinical presentation for CE
A
- Saddle anesthesia
- Bowel incontinence, bladder retention
- Reduced sphincter tone
- Erectile dysfunction
- Bilateral sciatica
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
34
Q
DDs for CE
A
- Conus medullaris syndrome
- Vertebral facture
- Peripheral neuropathy
- Mechanical back pain
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
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
37
Q
Components of a GCS
A
- Motor (6)
- Verbal (5)
- Eyes (4)
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
39
Q
Verbal points of a GCS score ?
A
- Orientated
- Confused conversation
- Inappropriate words
- Incomprehensible words
- None
40
Q
Eye points of a GCS score ?
A
- Spontaneous
- In response to speech
- In response to pain
- None
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
