Neurology Flashcards

1
Q

what are some red flags in a headache history?

A
  • new onset headache + history of cancer
  • cluster headache
  • seizures
  • altered conciousness/ memory/ confusion/ coordination
  • papilloedema
  • abnormal neurological examination
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2
Q

features of a migraine

A
  • 4-72 hours
  • must occur at least 5 times for diagnosis
  • painful, unilateral, pulsating, aggravated by routine physical activity
  • associated with nausea, photophobia, phonophobia
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3
Q

features of a tension headache

A
  • 30 mins- 7 days
  • bilateral pressing pain, not aggravated by routine physical activity
  • no nausea/ vomiting
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4
Q

features of a cluster headache

A
  • 15-180 minutes
  • severe unilateral orbital/ supraorbital pain
  • accompanied by ipsilateral cranial autonomic features and a sense of restlessness/ agitation
  • attacks occur in a ‘cluster’ then are separated by a ‘pain free’ period
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5
Q

features of trigeminal neuralgia

A
  • unilateral face pain in the distribution of the trigeminal nerve
  • lasts up to 2 minutes
  • like an electric shock
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6
Q

which headaches are classed as primary headaches?

A

migraine, cluster and tension

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7
Q

how are primary headaches treated?

A
- lifestyle modification 
pharmacological:
- oral triptans- NSAIDS/ paracetamol 
- anti-emetics
- topiramate/ propanolol 
- botulinum toxin injections
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8
Q

features of idiopathic intercranial hypertension?

A
  • pain is worse on walking, coughing, sneezing and straining
  • nausea and vomiting
  • pappiloedema
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9
Q

how is idiopathic intercranial hypertension treated?

A

acetazolamide
topiramate
diuretics

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10
Q

features of GCA

A
new onset headache
localised pain 
tenderness 
jaw claudication
visual disturbance
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11
Q

treatment of giant cell arteritis

A

prednisolone

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12
Q

features of medication overuse headache

A
  • headache present over 15 days/ month
  • caused by regular use of drugs (more than 3 months)
  • headaches worse during drug use
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13
Q

clinical features of MS

A
  • more common in females (usual age around 30)
  • monosymptomatic- most commonly optic neuritis
  • symptoms worsen on heat/ exercise
  • relapsing/ remitting- monosymptomatic followed by a period of no symptoms
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14
Q

diagnosis of MS

A
  • clinical
  • lesions disseminated in time and space attributed to no other known cause
  • MRI- identifies plaques
  • CSF- oligoclonal bands of IgG on electrophoresis
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15
Q

treatment of MS

A
  • vitamin D supplements
  • methylprednisolone to treat relapses
  • IFN- 1b and IFN 1a to decrease relapses
  • monoclonal antibodies- alemuzumab/ rituximab
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16
Q

what is myasthenia gravis?

A

autoimmune disease in which antibodies to nicotinic acetylcholine receptors are produced

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17
Q

clinical presentation of myasthenia gravis?

A
  • muscular weakness/ fatigue
  • ‘moves down’ e.g. symptoms begin extra ocularly and progress down the body towards the trunk
  • ptosis, diplopia, myasthenic snarl
  • voice fades on counting to 50
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18
Q

how is myasthenia gravis diagnosed?

A
  • anti-AChR antibodies found in 90%

anti- muscle specific Kinase (MuSK) antibodies

Large thymus/ clusters of immune cells in thymus - Thymomas (tumours)

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19
Q

treatment of myasthenia gravis?

A
  • symptom control- anticholinesterase medication= pyridostigmine
  • treat relapses with prednisolone +azathioprine/ methotrexate
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20
Q

what can exacerbate symptoms in myasthenia gravis?

A
  • pregnancy
  • hypokalaemia
  • infection
  • drugs- tetracycline, quinine, B-blockers
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21
Q

how is MND distinguished from MS and polyneuropathies?

A

affects UMN and LMN, but NO sensory loss or sphincter disturbance

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22
Q

clinical presentation of amyotrophic lateral sclerosis (ALS)

A
  • loss of motor neurons in motor cortex and anterior horn of spinal cord
  • weakness + UMN signs (upgoing plantars etc) +LMN wasting/ fasciculations
  • split hand sign- thumbs side of the hand seems to separate from the rest due to excessive wasting
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23
Q

clinical presentation of progressive bulbar palsy

A
  • cranial nerves IX-XII
  • LMN lesion of the tongue and muscles and talking -results in a flaccid, fasciculating tongue, absent jaw jerk, speech changes- quiet, horse, nasal
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24
Q

clinical presentation of progressive muscular atrophy

A
  • anterior horn cell lesions only
  • LMN only
  • affects distal muscle groups before proximal
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25
clinical presentation of primary lateral sclerosis
- loss of betz cells in motor cortex - UMN signs - spastic leg weakness and pseudo-bulbar palsy - no cognitive decline
26
How is MND generally diagnosed?
clinical findings and EMG/ nerve conduction studies
27
what is the El Escorial Criteria for the diagnosis of ALS?
- signs of LMN and UMN degeneration - progressive spread of signs together with the ABSENCE of: - - elctrophysiological evidence of other disease processes that may explain the signs - neuroimaging evidence of other disease pocess that may explain the observed signs
28
management of MND
- riluzole- extends life by around 3 month - baclofen for spasms - PEG tube for feeding if needed
29
UMN signs
``` weakness brisk reflexes hypertoni upgoing plantars (positive babinski) clonus ```
30
LMN signs
``` weakness depressed/ absent reflexes decreased tone wasting fasciculations ```
31
what is Guillain-Barre syndrome?
acute, inflammatory, demyelinating, ascending polyneuropathy that affects the PNS following an upper respiratory tract infection/ GI infection
32
what are some common infections that can trigger GBS?
- campylobacter jejuni - CMV - herpes zoster - EBV - HIV
33
clinical features of GBS
- post infection - symmetrical, ascending muscle weakness, begninning in the distal limb muscles and progresses proximally - loss of reflexes, neuropathic pain and autonomic dysfunction - can also affect respiratory muscles
34
diagnosis of GBS
- nerve conduction studies | - lumbar puncture- CSF- high proteins, normal WCC
35
how is GBS managed?
- IV immunoglobulin (IVIg) for 5 days | - monitor ventilation
36
clinical features of Huntingtons
- chorea- jerky, explosive, figidity movements - dysarthria, dysphagia, abnormal eye movements - dementia
37
what is the difference between spinal cord and spinal root compression?
spinal cord compression- myelopathy with UMN spinal root compression- radiculopathy with LMN
38
Clinical features of a subarachnoid haemorrhage
- thunderclap headache/ sudden onset severe headache - vomiting - collapse - seizures
39
clinical signs of a subarachnoid haemorrhage
- neck stiffness (Kernigs sign) - retinal bleeds - photophobia
40
diagnosis of SAH
star on CT
41
management of SAH
- surgery- endovascular coiling - maintain cerebral perfusion - nimodipine
42
features of a subdrual haematoma
- fluctuating conciousness - bleeding from bridging veins - symptoms occur late- a while after the initial injury
43
features of an extradural haematoma
- traumatic skull fracture | - lucid internal for a few days after injury
44
what is Lhermitte's phenomenon?
Neck flexion brings on a sudden sensation of an electric shock running down your spine Sign of MS
45
What is Uhthoffs phenomenon?
Temporary worsening of symptoms caused by an increase in temperature (e.g. - MS patient in hot bath)
46
what is clinically located syndrome?
First episode of MS characteristics that must last 24 hours. first attack of demyelination A diagnosis of MS can be made afterwards if the MRI shows lesions similar to those of MS
47
what is secondary progressive MS?
SPMS follows relapsing remitting. Relapsing remitting will transition into progressive worsening of neurological functioning
48
what is primary progressive MS?
Worsening of neurological functioning from the onset of symptoms, without early relapses or remissions 15% of diagnosis
49
What is relapsing remitting MS?
clearly defined attacks of new or increasing neurologic symptoms. These attacks – also called relapses or exacerbations – are followed by periods of partial or complete recovery (remissions). During remissions, there may be no symptoms, and no apparent progression of the disease
50
describe GCS scoring
Eye Opening (E) ``` 4 = spontaneous 3 = to sound 2 = to pressure 1 = none NT = not testable ``` Verbal Response (V) ``` 5 = orientated 4 = confused 3 = words, but not coherent 2 = sounds, but no words 1 = none NT = not testable ``` Motor Response (M) ``` 6 = obeys command 5 = localizing 4 = normal flexion 3 = abnormal flexion 2 = extension 1 = none NT = not testable ```
51
what condition is due to a CCG repeat?
fragile X syndrome
52
headache red flags
1) Sudden onset + severe 2) Age >50 3) Neck pain/stiffness, photophobia 4) Fever 5) Papilloedema 6) New onset neuro deficit 7) Vomiting 8) Dizziness and visual disturbances / atypical aura (over an hour)
53
what is giant cell arteritis?
Granulomatous medium/large vessel vasculitis | large vessel vasculitis of the head, scalp, arms, neck
54
what is a common association with GCA?
Polymyalgia Rheumatica - (neck, shoulders,back,hip) 1) Stiffness 2) Aching 3) Pain Jaw/ Tongue claudication Fever Headache
55
what anaemia is seen in GCA?
normocytic normochromic
56
what is the difference between a facial palsy caused by an upper or lower motor neurone lesion?
Upper motor neurone lesion spares the upper head e.g 'wrinkle forehead/ raise eyebrows'
57
what is Bells palsy?
Lower motor neurone palsy of the facial nerve (7th) Causing: 1) Facial droop on one side of the face 2) Cant close one eyelid 3) flat wrinkles on one side of forehead
58
how is Bells palsy diagnosed?
diagnosis of exclusion- rule out other possible causes
59
management of Bells palsy
- eye drops - wear sunglasses - corticosteroids- prednisolone
60
median nerve palsy
C6-T1 | carpal tunnel syndrome
61
ulnar nerve palsy
C7-T1 claw hand weakness/ wasting of medial wrist flexors
62
radial nerve palsy
C5-T1 | wrist and finger drop
63
Lat. cutaneous nerve of the thigh palsy
L2-L3 | meralgia paraesthesia- lateral burning thigh pain
64
sciatic nerve palsy
L4-S3 | foot drop
65
common peroneal nerve palsy
L4-S1 | foot drop, weak dorsiflexion, sensory loss
66
tibial nerve palsy
L4-S3 | failure of plantarflexion (tiptoes)
67
in which type of myopathy does spontaneous pain at rest occur?
inflammatory myopathy
68
which types of myopathy have a rapid onset?
toxic, drug or metabolic myopathies
69
what myopathy does pain on exercise relate to?
- ischeamia/ metabolic myopathy (McArdle's disease)
70
what myopathy does 'firm; muscles imply?
pseudo-hypertrophic muscular dystrophies (Duchenne's)
71
how does Duchene's muscular dystrophy present?
- young (around 4) - clumsy walking - diffuclty in standing - progresses to respiratory failure - pseudohypertrophy is also seen- in the calves
72
what marker is significantly raised in Duchennes?
serum creatinine kinase (over 40 times)
73
what is the inheritance pattern seen in duchenne's and beckers' muscular dystrophy?
x- linked recessive
74
how does myotonic dystrophy present?
- 20-40 years old - distal weakness (hand/foot drop) - weak sternocleidomastoids - facial weakness - cataracts - develop respiratory and cardiac problems
75
clinical presentation of inflammatory myopathies
- weakness of quadriceps, finger flexors | - poor response to therapy
76
drug causes of myopathy
alcohol, statins, steroids, chloroquine, zidovudine, vincristine, cocaine
77
clinical features of facioscapulohumeral muscular dystrophy?
- onset 12-14 - inabiltiy to puff out cheeks - cant raise arms over head - foot drop - scapular winging
78
what is dermatomyositis?
insidious onset of progressive symmetrical proximal muscle weakness plus 'skin signs' macular rash, purple eyelids
79
how are polymyositis and dermatomyositis investigated?
- ALT, AST, LDH, CK all raised - muscle biopsy confirms diagnosis - MRI shows some muscle oedema
80
how are polymyositis and dermatomyositis managed?
prednisolone | use hydroxychloroquine in dermatomyositis
81
what is status epilepticus?
a seizure lasting more than 30 minutes or repeated seizures without regaining consciousness
82
how is a diagnosis of status epilepticus confirmed?
EEG
83
how is status epilepticus managed?
- lorazepam - buccal midazolam - phenytoin infusion - dexamethasone
84
what is myasthenic crisis?
life-threatening weakness of the respiratory muscles during relapse
85
how is a myasthenic crisis monitored and treated?
- monitor FVC - treat with plasmapheresis (removes AChR antibodies from circulation) or give IVIg and identify and treat trigger of relapse (e.g. infection, medication)
86
how is the femoral nerve root tested?
L1,L2,L3 - iliopsoas- flex hip against resistance with knee flexed L2,L3,L4- quadriceps femoris- extend knee against resistance
87
how is the obturator nerve root tested?
L2,L3,L4- hip adductors- adduct leg against resistance
88
how is the inferior gluteal nerve tested?
L5,S1,S2- gluteus maximus- hip extension (bury heel into bed)
89
how is the superior gluteal nerve tested?
L4, L5, S1- gluteus maximum and minimus- abduction and internal hip rotation with leg flexed at hip and knee
90
Where do you test sensation in the following dermatomes on the arm? C5-T2
C5 - Over deltoid C6 - index finger C7 - middle finger C8 - little finger T1 - inside arm T2 - apex of axilla
91
Where do you test sensation in the following dermatomes on the leg? L2-S2
L2 - anterior medial thigh L3 - over knee L4 - medial tibia L5 - dorsum of foot running to big toe S1 - lateral heel S2 - popliteal fossa
92
Where do you test movement in the following myotomes on the arm? C5-T1
C5 - shoulder abduction C6 - elbow flexion C7 - elbow extension C8 - finger flexion T1 - finger abduction
93
Where do you test movement in the following myotomes on the leg? L2-S2
L2- Hip flexion L3- Knee extension L4- Ankle dorsiflexion L5- Extension of big toe S1- Ankle plantar flexion S2- Knee flexion
94
What muscles does the radial nerve innervate
Triceps and finger extensors
95
What muscles do the median nerve innervate?
LOAF Lateral 2 lumbricals Oppenens brevis Abductor pollicis brevis Flexor pollicis brevis
96
What muscles do the ulnar nerve innervate?
Intrinsic muscles of the hand, lumbricals, hypothenar and interossei
97
What nerve is responsible for: Finger flexion? Finger extension? Finger abduction?
Median Radial Ulnar
98
What is the most common winged scapula nerve lesion?
Long thoracic nerve (serratus anterior)
99
What nerve is responsible for the following movements? knee extension knee flexion ankle dorsiflexion Big toe extension ankle plantar flexion
knee extension - femoral L3 knee flexion - sciatic/tibial L5, S1/2 ankle dorsiflexion - peroneal L4 Big toe extension - peroneal L5 ankle plantar flexion - tibial S1
100
Name some foot drop differentials?
Muscle: myopathy Nerve: peroneal nerve, sciatic nerve Root: L4/5 Anterior horn: MND Brain: parasaggital mengingioma
101
Which lobe is Brocas area in and what is its function?
region in the frontal lobe of the dominant hemisphere, usually the left, of the brain with functions linked to speech production
102
Which lobe is Wernicke's area in and what is its function?
located in the temporal lobe on the left side of the brain and is responsible for the comprehension of speech
103
What are Kernigs and Brudzinkis sign?
- Kernig's (inability to straighten knee when hip flexed 90 degrees) - Brudzinski's- neck stiffness - flex neck and knee+hip flex too
104
Symptoms of Optic Neuritis?
1) Reduced visual acuity over days 2) Pain on moving eye 3) Exacerbated by heat/exercise 4) Afferent pupillary defect 5) Dyschromatopsia (especially red)
105
How does Huntingtons occur?
autosomal dominant 1) Chromosome 4 produces Huntingtin protein 2) Mutation to the Huntington gene on chromosome 4 results in CAG nucleotide repeats 3) This leads to an abnormal Huntingtin protein & neurodegenerative disorder
106
What type of hypersensitivity reaction is Myasthenia Gravis and Multiple Sclerosis?
MG - type II (antibody mediated - AChR / MuSK) MS - type IV (cell-mediated- T cell crosses brain barrier, activated by myelin, sends signal to allow more T cells across barrier)
107
what are 3 risk factors of MS?
Female Vit D deficiency HLA-DR2
108
What is Charcots Neurological Triad?
1) Dysarthria (dysfunctional eating, talking, swallowing) 2) intention tremor (muscle weakness, spasms, ataxia, paralysis) 3) Nystagmus (Optic Neuritis, greying of vision, pain, double vision) Linked to MS
109
What visual defects are caused by: Temporal lesions?
contralateral superior quadranopia PITS (Parietal-Inferior, Temporal-Superior)
110
What visual defects are caused by: Parietal lesions?
contralateral inferior quadranopia PITS (Parietal-Inferior, Temporal-Superior)
111
What visual defects are caused by: Diabetes Insipidus due to craniopharyngioma
lower bitemporal hemianopia
112
What visual defects are caused by: Pituitary macroadenoma
Upper bitemporal hemianopia
113
What visual defects are caused by: Occipital cortex lesion?
Macula sparing homonymous hemianopia
114
What visual defects are caused by: compression of the optic chiasm
Bitemporal hemianopia
115
treatment of migraines
NSAIDS- ketoprofen, aspirin - triptans (5HT agonists)- rizatriptan, sumatriptan 1st line- propanolol, amitryptilline, CCB's 2nd line- valporate, pizotifen, gabapentin
116
treatment of trigeminal neuralgia
carbamazepine, lamotrigine, phenytoin | surgery
117
causes of spinal cord compression
- secondary malignancy- breast, lung, prostate, thyroid, kidney - infection- epidural abscess - cervical disc collapse - haematoma - intrinsic cord tumour - atlanto-axial subluxation - myeloma
118
treatment of spinal cord compression
* If malignancy – give dexamethasone IV while waiting for radio/chemotherapy ± decompressive laminectomy * Epidural abscess – surgical decompression and abx
119
what is cauda equina and how does it present?
- damage to the spine at or distal to L1 - presents with leg weakness, back pain, radicular pain down legs, asymmetrical, atorphic, arereflexic paralysis of legs, sensory loss in root distribution, decreased sphincter tone
120
causes of cauda equina syndrome
- trauma - congenital lumbar disc disease - lumbosacral nerve lesions - lumbar disc prolapse
121
examples of primary malignant brain tumours
- glioma - embryonal tumours- medulloblastoma - lymphoma
122
examples of benign brain tumours
- meningioma | - neurofibroma
123
what cancers metastasise to the brain?
- bronchial - breast - stomach - prostate - thyroid - kidney
124
what are the clinical features of a brain tumour and what causes these?
- neurological deficit- due to mass effect of tumour and surrounding cerebral oedema - raised ICP- results in headache, vomiting and papilloedema - epilepsy
125
how can a brain tumour cause respiratory depression?
raised ICP- brain is displaced downwards, which puts pressure on the brainstem. This causes drowsiness, resulting in respiratory depression, braycardia and death
126
differential diagnosis for a brain mass
- tumour - cerebral abcess - tuberculoma - subdural haematoma - intracranial haematoma
127
what organisms can cause meningitis
- meningococcus or pneumococcus less common: - hemophilus influenzae - listeria monocytogenes - HSV - VZV
128
differential diagnosis for meningitis
- malaria - encephalitis - septicaemia - tetanus
129
what are the clinical features of meningitis (early and later)?
early- headache, fever, leg pains, cold peripheries, palor later: - meningism- neck stiffness, photophobia, Kernigs sign - decreased GCS, come - seizures and focal CNS signs - non-blanching petechial rash - prolonged CRT
130
Management of meningitis
- early Abx- cefotaxime and ampicillin - dexamethasone - fluid rescucitation - contact tracing prophylaxis- rifampicin ciprofloxacin
131
lumbar puncture- differences in: - appearance - protein between bacterial, tuberculous and viral meningitis
appearance: - bacterial- turbid - tuberculous- fibrin web - viral- clear protein (g/L) - bacterial- >1.5 - tuberculous- 1-5 - viral- <1
132
what is encephalitis?
inflammation of the brain parenchyma
133
how does encephalitis present?
- abnormal cerebral function with altered mental status, motor and sensory deficits - fever, headache, drowsiness - focal neurological signs - seizures
134
causes of encephalitis?
look for history of recent travel/ animal bite usually viral: - herpes simplex - CMV - EBV - VZV - HIV - measles non-viral causes: - bacterial meningitis - TB - malaria - listeria
135
investigations in encephalitis
- CT/ MRI - viral serology of CSF and blood - EEG
136
Tx of encephalitis
IV acyclovir
137
what is shingles?
re-activation of the herpes zoster virus after a previous primary infection with chickenpox virus remains dormant in dorsal root ganglia/ cranial nerve ganglia
138
what is the dermatome distribution seen in shingles?
- rash- papules and vesicles - pain and tingling - lower thoracic dermatomes and opthalmic division of trigeminal nerve
139
treatment of shingles
oral acyclovir
140
what is the most common complication in shingles and how is it treated?
- post-herpetic neuralgia (PHN) | - tx- carbamazepine
141
features of an ataxic gait
- wide based - falls - cannot walk heel to toe - worse in dark/ with eyes closed
142
2 main causes of an ataxic gait
- cerebellar dysfunction | - proprioceptive issues
143
what are the cerebellar causes of an ataxic gait?
- MS - posterior fossa tumour - alcohol - phenytoin toxicity deficit is ipsilateral to cerebellar lesion
144
what are the features of cerebellar syndrome?
ataxia plus nystagmus
145
what are the proprioceptive causes of an ataxic gait?
- sensory neuropathies (low B12) | - inner ear problem- affecting the vestibular system
146
what test helps you distinguish between proprioceptive and cerebellar causes of ataxic gait?
- if they can walk normally with their eyes open but not when they close= proprioceptive - if the problem is there regardless= cerebellar
147
what are the features and cause of a circumduction (spastic) gait?
- features- stiff gait, circumduction of legs (scuffing of the toes of the shoes) - cause- stroke (hemiplegia)
148
what are the features and cause of a shuffling (extra-pyramidal) gait?
- features- flexed posture, shuffling feet, postural instability, difficulty initiating movements - causes- Parkinsons disease
149
what is and what are the causes of an antalgic gait?
- limping | - MSK- pain
150
what are the features and causes of a high stepping gait?
- features- trip over often, lift feet high to avoid tripping over - cause- common peroneal palsy- foot drop
151
what are the features and causes of trendelenberg gait?
- features- unstable hip, 'sound side sags' on tendelenberg test - causes- hip dislocation, DDH
152
what are the features and causes of an apraxic gait?
- features- 'feet glued to floor', wide based unsteady gait with a tendency to fall - causes- normal pressure hydrocephalus, multi-infarct states, Alzheimers
153
How does mononeuritis multiplex present and what are some causes?
- individual nerves picked off randomly – wrist drop, leg numbness, foot drop - Subacute presentation – months rather than years - Inflammatory/immune mediated Causes –inflammation of the vasa nervorum can block off the blood supply to the nerve causing sudden deficit - Vasculitis (wegner’s, PAN, RA), sarcoidosis
154
causes of a myasthenic crisis
- infection - progression of disease - under/overdosing medication
155
what is the definition of a coma/ brain death?
unarousable unresponsiveness
156
what are lateralising signs in neurology?
- occur from one hemisphere of the brain but not another
157
what causes a fixed dilated pupil?
- 3rd nerve palsy
158
metabolic causes of a coma
- drugs, posioning - hypo/hyperglycaemia (HONK, ketoacidosis) - hypoxia - CO2 narcosis- COPD- if hypoxic drive decreases, CO2 builds up - septicaemia - hypothermia - addisonian crisis - encephalopathy
159
neurological causes of coma
- trauma - finection- meningitis, encephalitis etc - trauma - vascular- stroke, haemorrhages etc - epilepsy
160
how is the unconscious patient managed?
ABC – life support IV access Stabilise cervical spine (especially if trauma is likely) Control any seizures – phenytoin loading etc Treat potential causes – IV glucose, thiamine, nalaxone if pupils small Brief collateral history and examination Vital signs and pupils checked often Investigations – Bloods, cultures, CXR, CT head Continually re-assess and plan investigations
161
what is the definition of vertigo?
an illusion of movement, often rotary, of the patient of their surroundings
162
causes of vertigo
- motion sickness - alcohol - benign positional vertigo - meniere's disease
163
how does acute glaucoma present?
- in elderly - constant aching pain develops rapidly around 1 eye - reduced vision, visual halos, nausea - red, congested eye, cloudy cornea, non-responsive dilated pupil, decreased acuity
164
how is acute glaucoma treated
IV acetazolamide
165
what are tardive syndromes and what causes them?
- Tardive = delayed onset, occurs due to chronic exposure to dopamine antagonists (antipsychotics, anti-emetics) - May be permanent – even once the causative medication has been stopped - Tardive dyskinesia – chewing and grimacing movements involving the face, mouth and tongue- common in schizophrenics or have been on long-term typical anti-psychotics - Tardive dystonia – twisting/turning of the limbs and back - Tardive myoclonic, tourettism and tremor can also occur
166
what is dysphasia?
impairment of language
167
what is dysarthria?
difficulty with articulation of speech- slurred speech
168
what is dysphonia?
difficulty with speech volume due to weakness of respiratory muscles or vocal cords (MG, GBS)
169
what is the difference between bulbar and pseudobulbar palsy?
psuedo- UMN - bulbar- LMN Pseudobulbar dysarthria – slow, nasal, effortful ‘hot potato’ voice Bulbar dysarthria – nasal speech due to paralysis of the palate
170
What is dysphagia?
difficulty swallowing
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what is Miller- Fisher syndrome?
related variant to GBS that affects the CNS and eye muscles characterised by opthalmoplegia and ataxia
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what is hydrocephalus and what are the 3 subtypes?
- Hydrocephalus = abnormal build-up of CSF around the brain Subtypes: - Congenital hydrocephalus – born with excess fluid on the brain - Acquired – develops at some point after birth due to injury or illness - Normal pressure hydrocephalus – uncommon and poorly understood, usually only develops in >60 year olds
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what causes congenital hydrocephalus?
- spina bifida | - infection during pregnancy (mumps, rubella)
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what causes acquired hydrocephalus?
develops after illness or injury (brain tumour/ head injury)
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causes of normal pressure hydrocephalus
- develops after head injury/ stroke
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symptoms of normal pressure hydrocephalus
- abnormal gait - urinary incontinence - dementia
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general symptoms of hydrocephalus
headache vomiting blurred vision difficulty walking
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how is hydrocephalus investigated?
- CT and MRI scans used to diagnose congenital and acquired hydrocephalus - NPH – diagnostic criteria = walking, mental ability and bladder control (important to diagnose NPF correctly because unlike Alzheimer’s the symptoms can be relieved with treatment)
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how is hydrocephalus managed?
- Vetriculo-peritoneal shunt – surgically implanted into the brain to drain away excess fluid - Endoscopic third ventriculostomy – alternative to shunt surgery – hole made in the floor of the third ventricle to allowed trapped CSF to escape to the surface where it can be re-absorbed
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what is Gelineau's syndrome?
Narcolepsy irresistible attacks of innaprorpiate sleep with vivid hypnogognic hallucinations and sleep paralysis
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treatment of Gelineau's syndrome
- regular sleeping routine - avoid excess caffiene and alcohol - pharmacological- methylphenidate/ modafinil
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what is cataplexy?
sudden loss of muscle tone while a person is awake leads to weakness and a loss of voluntary muscle control. It is often triggered by sudden, strong emotions such as laughter, fear, anger, stress, or excitement
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treatment of cataplexy
sodium oxybate
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inheritance pattern in neurofibromatosis
autosomal dominant
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clinical signs of neurofibromatosis T1
- cafe-au-lait spots- coffee coloured patches seen on skin in 1st year of life - freckling - dermal neurofibromas lisch nodules -
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complications of neurofibromatosis T1
- mild learning disabilitiy - nerve root compresssion - GI bleeds - bone lesions - increased risk of epilepsy
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what is neurofibromatosis?
genetic disorder of the nervous system that results in tumours forming on nerves
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what are T1 and T2 neurofibromatosis also referred to as?
T1- recklinghausen disease T2- bilateral acoustic neurofibromatosis
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how can T2 neurofibromatosis be differentiated from T1?
- characterised by multiple tumours on the cranial and spinal nerves - first symptoms occur in early 20's- usually hearing loss
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treatment of neurofibromatosis
- surgery to remove problem tumours - chemotherapy - physical therapy
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describe the history, symptoms before, during and after in syncope
history- previous faints, poor oral intake, PMH before- hot, dizzy, visual crowding, visual blurring, ringing in ears, pale during- LoC, seconds to minutes, occasional jerks, pale, clammy, no tongue biting, no incontinence after- quick recovery, no confusion
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describe the history, symptoms before, during and after a seizure
History- childhood development, head injury, neurosurgery, stroke, malignancy before- aura during- 2-3 mins LoC, convulsions depending on type of seizure, automatisms (lip smacking), eye deviation, tongue biting, urinary incontinence after- post ictal confusion, disorientated, headache
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describe the history, symptoms before, during and after in a NEAD
history- MUS, history of trauma before- aura during- can last a long time, symptoms not localisable, pelvic thrusting, screaming, crying, responsive (sometimes), thrashing around after- atypically quick, emotionally labile, minimal confusion
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what is an essential tremor?
element of postural tremor which continues through movement (e..g hands shaking when drinking a cup of tea) does not occur at rest
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how are essential tremors managed?
propanolol/ primidone/ pregabalin/ gabapentin
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what other conditions can present with Parkinsonism?
- idiopathic parkinsons disease - vascular parkinsonism - normal pressure hydrocephalus - Parkinsons plus (progressive supranuclear palsy, multiple system atrophy) - iatrogenic
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how does Parkinsonism present?
- shuffling gait - pill rolling tremor - bradycardia - cogwheel rigidity - micrograhpia - cramping - non-motor symptoms- mood, sleep etc
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how is REM sleep behaviour disorder treated?
clonazepam/ melatonin
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what autonomic symptoms are associated with parkinsonism?
``` orthostatic hypotension constipation nausea vomiting heat intolerance urinary frequency urinary incontinence nocturia sexual dysfunction ```
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what presents with worsening symptoms with movement and stress, but symptom relief upon sleep and alcohol consumption?
essential tremor
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what mutations are seen in familial MND?
SOD1- association between this and fronto-temporal dementia | C9ORF72
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mutation seen in Huntingtons disease
- chromosome 4 - autosomal dominant - CAG trinucleotide repeat
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what is Hoffman's sign and what is it commonly seen in?
flicking of the patient’s middle finger illicts contraction of the thumb (UMN sign), seen in MS
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other than huntingtons, what else can cause chroea?
- wilsons - ataxic telanglectasia - SLE - rheumatic fever - OCP, L-dopa - pregnancy - thyrotoxicosis - polycythaemia rubra vera - CO poisoning - cerebralvascular disease
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what medications must be avoided in Parkinsons?
anti-physcotic meds (e.g. halopiderol)- anti-dopaminergic