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
Diagnosis of myelopathy
- 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
Treatment for myelopathy
- If malignancy – IV dexamethasone (high dose) reduced inflammation/oedema around malignancy and improves outcome
27
What is cauda equine syndrome ?
- A medical emergency where the nerve roots of the cauda equina become compressed
28
What do the nerves of the cauda equina supply ?
- 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
Common cause of cauda equina ?
- Herniation at L4/5 and L5/S1
30
Aetiology for cauda equina ?
- Herniation at L4/5 and L5/S1
- Tumour/metastases
- Trauma
- Infection Spondylolisthesis
- Post-op haematoma
31
Pathophysiology of CE
- 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
Clinical presentation for CE
- Saddle anesthesia
- Bowel incontinence, bladder retention
- Reduced sphincter tone
- Erectile dysfunction
- Bilateral sciatica
33
Red Flags in CE and DDs
- 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
DDs for CE
- Conus medullaris syndrome
- Vertebral facture
- Peripheral neuropathy
- Mechanical back pain
35
DD of CE
- 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
Treatment for CE
- Refer to neurosurgeon ASAP to relieve pressure or risk irreversible paralysis/ sensory loss/incontinence
- Microdiscectomy
- Epidural steroid injection
- Surgical spine fixation
- Spinal fusion
37
Components of a GCS
- Motor (6)
- Verbal (5)
- Eyes (4)
38
Motor points of a GCS score ?
- Obeying commands
- Localising to pain
- Withdrawing to pain
- Flexor response to pain
- Extensor response to pain
- No response to pain
39
Verbal points of a GCS score ?
- Orientated
- Confused conversation
- Inappropriate words
- Incomprehensible words
- None
40
Eye points of a GCS score ?
- Spontaneous
- In response to speech
- In response to pain
- None
41
What is delirium ?
- An acute confusional state seen commonly in elderly patients
- Characterised by disturbance of consciousness, perception, sleep-wake cycle, emption and cognition
42
Aetiology of Delirium
- 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
Symptoms of delirium
- Inattention
- Altered consciousness
- Altered sleep wake cycle
- Hallucinations and mood changes
- Hypoactive: apathy, withdrawal and quite
- Hyperactive: agitation, delusions and disorientation
44
Investigations for delirium
- 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
Medication treatment for extremely agitated delirious patients
- Haloperidol or olanzapine
46
Clinical features of delirium
- 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
RFs for delirium
- Dementia/previous cognitive impairment
- Hip fracture
- Acute illness
- Psychological agitation e.g. pain
48
What is Guillain-Barre Syndrome ?
- An acute, autoimmune, inflammatory, demyelinating ascending polyneuropathy affecting the peripheral nervous system (Schwann cells) following an URT or GI infection
49
Clinical presentation of Guillain-Barre Syndrome
- Paraesthesia without sensory loss
- Absence of deep tendon reflexes
- Increased CSF albumin
50
Peak incidence of Guillain-Barre Syndrome
- 15-35yo and 50-75yo
- MC acute polyneuropathy
- More common in males
51
Causes of Guillain-Barre Syndrome
- MCC – Campylobacter jejuni
- Cytomegalovirus
- Mycoplasma
- Zoster
- HIV
- EBV
- In some cases idiopathic
52
Pathophysiology of GBS
- 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
Clinical presentation Guillain-Barre Syndrome
- 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
Diagnosis of GBS
- Nerve condition studies
- Lumbar puncture done at L4 – raised protein but normal CSF count
- Spirometry
- Immunoglobulin levels
55
Treatment for GBS
- IV immunoglobulin for 5 days – reduces duration and severity of paralysis
- Plasma exchange
- Supportive Management
- Reduce VTE risk, swallowing, neuropathic pain, depression,
56
How do you treat neuropathic pain ?
- 1st Gabapentin
- Carbamazepine
- Tramadol
57
Prognosis for GBS
- 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
What is Brown-Seqard Syndrome ?
- Lateral hemisection of the spinal cord
59
What are the presenting features of Brown-Seqard Syndrome ?
- 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
Stroke with quadriplegia and small reactive pupils. History of HTN
- Pontine haemorrhage
61
What is autonomic dysreflexia
- 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
A painful 3rd nerve palsy is caused by what until proven otherwise ?
- Posterior communicating artery aneurysm
63
Used to treat oedema around tumours in the CNS ?
- Dexamethasone
64
What is ROSIER used for ?
- Recognition of strokes in the emergency room
- Used to differentiate between strokes and stroke mimics
65
Tools used in strokes
- ROSIER – stokes in the emergency room
- ABCD2 – risk of stoke after TIA
- CHA2DS2-VASc – likelihood of stroke secondary to AF
66
Used to identify patients at risk of pressure sores
- Waterlow score
67
Screening tools for dementia
- 10 point cognitive score (10-CS)
- 6 item cognitive impairment test (6CIT)
68
What is normal ICP
- 7-15 in adults in a supine position
69
What is cerebral perfusion pressure ?
- Net pressure gradient causing blood flow to the brain
- CPP = mean arterial pressure
70
What are the causes of raised ICP
- Idiopathic
- Trauma
- Infection
- Tumours
- Hydrocephalus
71
Features of ICP
- Headaches
- Vomiting
- Reduce levels of consciousness
- Papilloedema
- Cushing’s triad
72
How is raised ICP investigate
- 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
How is raised ICP managed ?
- 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
How will a 3rd nerve palsy present ?
- Down and out eye
- Ptosis
- Pupil may be dilated (surgical 3rd nerve palsy)
75
Causes of a 3rd nerve palsy
- DM
- Vasculitis e.g. temporal arteritis or SLE
- Posterior communicating artery aneurysm
- MS
76
What factors would suggest delirium vs dementia ?
- 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
What factors would suggest depression over dementia ?
- 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
Medications for Parkinson's
- 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
Side effects of Levodopa
- Dry mouth
- Anorexia
- Palpitations
- Postural hypotension
- Psychosis
- Dyskinesia at peak dose
80
SEs of dopamine receptor agonists
- Impulse control disorders
- Excessive daytime somnolence
- Hallucinations
- Nasal congestions
- Postural hypotension
81
Medications for dementia
- The three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine)
- Donepezil – contraindicated with bradycardia – adverse effects include insomnia
82
Hereditary for Essential tremor
- Autosomal dominant
83
Medication of essential tremor
- Propranolol is 1st line
- Primidone is sometimes used
84
Typical Presentation of Vascular Dementia
- Stepwise deterioration of cognitive function
- Focal neurological abnormalities e.g. visual disturbances
- Attention and concentration difficulty
- Seizures
- Memory, gait, speech and emotional disturbance
85
NINDS-AIREN criteria of vascular dementia
- 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
Psychological Therapies Dementia
- 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
Features suggesting MND
- 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
Most common type of MND
- Amyotrophic lateral sclerosis
89
Medications for MND
- Riluzole
- Baclofen for muscle spasticity
- Non-invasive ventilation at night
- PEG
90
McDonald criteria for MS an individual must have:
- 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
Most common presentation in MS
- Optic neuritis
- Demyelination of the of the optic nerve presenting with unilateral reduced vision developing over hours to days
92
Key features of optic neuritis
- 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
MS focal weakness symptoms
- Incontinence
- Horner syndrome
- Facial nerve palsy
- Limb paralysis
94
MS focal sensory symptoms
- Trigeminal neuralgia
- Numbness
- Paraesthesia
- Lhermitte’s sign
95
What is Lhermitte’s sign
- 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
What is Hoffman’s sign
- An involuntary flexion movement of the thumb and or the index finger when the examiner flicks the fingernail of the middle finger down
97
What is Romberg’s test ?
- Lose balance when standing with their eyes closed
98
What are the types of MS ?
- Clinically isolated syndrome
- Relapsing remitting
- Secondary progressive
- Primary progressive
99
What is Gowers sign
- 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
Management of Muscular Dystrophy
- Oral steroids slow progression
- Creatine supplementation can give slight improvement of muscle strength
