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Hayders Phase 2A > Neuro > Flashcards

Neuro Flashcards

1
Q

what are the different types of sensory neurons and what do they carry

A

Alpha- heavily myelinated, proprioception
Beta- less myelinated, crude touch pressure vibration
Delta- least myelinated, cold temperature, sharp pain
C fibres, unmyelinated- hot tempreture dull pain

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2
Q

what are the different types of nerve damage

A

demylination- post diptheria neuropathy, GB sybdrome
axonal damage- denegerative, toxic neuropathy (commonest type
compression- Pressure- entrapmentt
Infarction- DM neuropathy
Inflammatory and granulomas- leprosy, granulomas

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3
Q

what is mononeuropathy and its causes

A

Neuropathy of 1 singular nerve, causes by trauma or entrapment

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4
Q

types of mono neuropathys

A 
Carpal tunnel syndrome
bells palsy
common peroneal nerve palsy
sciatica 
ulner nerve palsy 
radial nerve palsy 
lateral cutaneous nerve of thigh- meralgia parasthesia
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5
Q

investigation and diagnosing mononeuropathys and mononeuropathy complex

A

nerve conduction studies and history

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6
Q

what is mono neuropathy complex and its cause

A 
neuropathy of a few specific nerves 
WARDSPLC
wengers 
aids 
rheumatoid
diabetes M 
Sarcoidosis 
Leprosy 
Carcinoma
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7
Q

what is polyneuropathy and its types of presentation

A

Disorder of peripheral nerves, can be acute or chronic, sensory or motor. commonest is sensory motor

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8
Q

sensory neuropathy presentation

A

parasthesia,
ataxia - test if ataxia is sensory or centeral, close eyes.
sensory loss

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9
Q

motor neuropathy presentation

A 
Weakness, paresis 
plegia, paralysis 
fasiculations, twictching. 
cramps
atrophy
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10
Q

Axonal Polyneuropathy, commonest type and its presentation

A

symmetrical sensory motor PN

starts ditsally as just sensory and becomes more proximal and more motor

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11
Q

causes of axonal PN

A 
DM, Renal failure, hyopthyroidism 
malignancy or polycythemia rubra vera 
Inflammatory, GB syndrome sarcoidosis 
Vit B12 deficiency 
Drugs, alcohol induced, metronidazole 
inherited, charcot mary tooth 
vasculitis- ANA and ANCA
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12
Q

commonest cause of neuropathy

A

Diabetic Neuropathy

then Chronic idiopathic axonal neuropathy- probablu inflamatory but unkown

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13
Q

commonest cause of demyelination

A

Chronic inflammatory immune mediated demyelination- autoimmune- (type of GBS)
then genetic causes like charcot mary tooth syndrome

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14
Q

what is Guillain barre syndrome

A

acute inflammatory demyelinating neuropathy, can be axonal- only affects peripheral nerves

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15
Q

causes and onset of Guillain barre syndrome

A

onset after infection, Campylobacter jejuni or cytomegalovirus, actual cause unknown could be vaccines

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16
Q

clinical features of Guillain barre syndrome

A

usually starts 1-3 weeks post infection. start with parastheis and weakness deveops proximally as time goes on and gets worst over 6 weeks then spontanously improves
affects proximal muscles body like trunk more
can deveopl respiratory muscle wekaness or autonomic signs like retention, bowel and bladder plus erectile dysfunction

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17
Q

diagnoses of Guillain barre syndrome

A

clinical based on history, can do nerve condction studies.

CSF protien elevated

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18
Q

management of Guillain barre syndrome

A

IV immunoglobulins improve prognosis

monitor for resp complications may need ventilation

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19
Q

General management for neuropathies

for vasculities or Guillain barre syndrome

A

Pain- amytriptyline or Gabapentin
balance- physiotherapy and occupational therapist, walking aid, retraining, foot care in neuropathies
GBS- IV Immunoglobulins
Vasculitis- steroids

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20
Q

commonest cause of brain tumour

A

Secondary tumour that has metastasised from elsewhere usually lung or breast

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21
Q

Types of brain tumour

A 
primary- Gliomas, commonest primary tumour
other types, meningioma
schwannoma, acoustic neuroma 
craniophangyoma- in pituitary 
Secondary
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22
Q

How does a brain tumour present

A

focal or non focal neurological defects- weakness, dysathia
Generalised or localised seizures
raised ICP will cause ICP headache and papilloedma

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23
Q

feautures of raised ICP hedache

A

headache, worst at night and in mornings, worst when lie down or cough or exercise.
relieved by vomiting,
assosiated with papilloedma
Dull pain behind eyes

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24
Q

Investigations for Brain tumour

A

CT or MRI, any new onset seizure = CT Scan

biopsy once confirmed its a tumour to see what kind of tumour it is and treatment options

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25
Q

How are Gliomas Classified

A 
WHO classification of primary Gliomas 
1 begin
2 slow growing
3 high grade 
4 commonest type- 12 month survivability
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26
Q

causes of primary brain tumours

A

usually no known cause
associated with ionising radiation at a young age
family history
immunosuppresssion

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27
Q

Treatment of brain tumour

A

Dexamethasone to reduces brain swelling and oedema
diuretics
Tumour resection or removal (awake craniotomy)
followed by radiotherapy and chemotherapy

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28
Q

what is motor neuron disease and what neurons does it affect or not affect

A

chronic degenerative disease affecting Upper and lower MNs. does not affect eyes.
does not affect sensory or sphincters

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29
Q

what is the prevalence likely age group and prognosis of MND

A

Prevalence 6 in 100,000
average onset 60
prognosis 2-4 years

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30
Q

types of MND

A

Amylotrophic lateral sclerosis- commonest
progressive bulbar palsy
progressive muscular atrophy
primary lateral sclerosis

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31
Q

Presentation of MND

A

Has both UMN and LMN lesions, no effect on eyes. fasiculations. spasticity. increased tone but weakness.
hyperreflexia
CXR shows raised diaghram bilaterally

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32
Q

Diagnosis of MND

A

clinical diagnoses
neurophysiology studies- confirms deinnervation
neruoimaging to exclude other causes

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33
Q

Managment of MND

A

MDT, Physio OT Dietican and social care
avoid chokcing due to dysphagia by belnding food or NG tube
monitor may need Ventilation due to diaphram and resp muscle paralysis
pain- analgesic ladder
drooling- propantheline
antiglutamatergic drugs- Riluzole ( drug that improves prognosis for ALS)

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34
Q

What is mysthenia gravis

A

autoimmune condition againts acetylecholen receptors AChR antibodies.
neuromuscular junction condition

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35
Q

mysthenia gravis signs and symproms

A

Increasing muscle fatigue, muscle weakness
fasiculations . gets worst as disease progresses
tender reflexes dissapear over time
sensory not affected.
ptosis, diplopia Extraoccular palsy
mysenthic gnarl

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36
Q

myasthenia gravis where do the symptoms start and where does it progress to

A

start at eyes, then face, neck trunk, limbs

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37
Q

assosiations of myasthenia gravis

A

women under 50 with other autoimmune disease

men over 50 withother autoimmune disease, rhematoid SLE and thymus hyperplasia in both

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38
Q

Investigations of Myasthenia gravis

A

Serology- Anti AChR antibodies
neurophysiology, muscle stimulation gets less after repeated stimulation
CT of thymus.
applying ice pack to closed eyelid for 2 mins= ptosis improves temporarly

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39
Q

Treatments of Myasthenia Gravis

1st and second line pharmacological

A

Anti acetylcholinesterase - pyridostigmine

2nd line is immune suppression- predniselone

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40
Q

treatment of myasthenia gravis

surgical

A

Thymectomy,

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41
Q

complications of myasthenia gravis,

A

myasthenic crisis- respiratory problems, dysphagia

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42
Q

what are the different kinds of headache

A

Primary - tension, cluster, migraine
secondary - meningitis SAH, GCA, ICP headache, medication overuse headache
Other/cranial neuropathy - trigeminal neuralgia

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43
Q

what are the different kinds of migraines

A

with auras- classic

without aura - common

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44
Q

classical migraine with auras features

A

2 attacks in a year.
has at least 1 aura: fully reversible visual or speech distubances
has 2 of: 1 Homonymus visual symptoms/unilateral sensory symptoms. 2 symptoms develop gradually, over 5 minutes. 3 each symptom lasts 5 to 60 minutes

headache usually unilateral throbbing following the auras. can be other character
Not attributable to other causes

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45
Q

common migraine without auras features

A

5 attacks in a year
onset of pain lasting 4-72 hours
has one of (photo and phonophobia) or (nausea and or vomiting)
has 2 of: unilateral, throbbing, moderate/severe, aggrivated by physical exertion
not attributable to other causes

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46
Q

Triggers for migraines are

A 
CHOCOLATE
hangover
orgasm 
cheese
oral contraception 
lie in/destressing
alcohol
exercise
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47
Q

Management of migraines

A

firstly if sudden onset, exlude thunderclap
education on avoiding triggers
prevention by B blockers, Proplanolol or Botulinum
migrane rescue treatment by triptans (seritonin receptor agonist), NSAIDs and Antiemetic

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48
Q

Tension headache features

A

Commonest type of headache.
30 mins to 7 days.
2 of the 4: Bilateral, Mild/Moderate, Tight banding (not throbbing), not aggravated by physical exertion
No nausea/vomiting or aura
either photophobia or phonophobia or neither but not both.
if occurs 12 in a year considered chronic

A sign is scalp tenderness

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49
Q

Triggerst of tension headache

A 
MCSCOLD
Missed meals
conflict
stress
clenched jaw
over exersion 
lack of sleep
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50
Q

Precipiants of tension headache

A

worry, noise, concentration visual effort

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51
Q

commonest cause of tension headache

A

medication overuse

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52
Q

management for tension headache

A

education, avoiding triggers
NSAIDs and analgesic withdraw.
massage, ice pack

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53
Q

Cluster Headache Features

A

rapid onset of very severe headache, usually in one eye causing bloodshot eye or watery. miosis, ptosis, rhinorrhea.
always unilateral.
occurs at any age, unknown cause
get attack everyday for 4-12 weeks then a few months to a year of then back again

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54
Q

Diagnostic criteria for cluster headache

A

at least 5 attacks,
occurring at least one a day or at max 8 per day
V/Severe unilateral pain, suborbital orbital or temporal
lasts 15-180 minutes
accompanied by ipsilateral autonomic features or restlessness

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55
Q

management for cluster headache

A

100% oxygen for 15 minutes an sumatriptans

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56
Q

Prevention for Cluster Headache

A

Verapamil (CCB), lithium

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57
Q

Trigeminal neuralgia diagnostic criteria

A

occurs in Trigeminal nerve lesion, doesn’t radiate further, usually maxillary or mandibular
ha 3 of the following:
sudden recurring, lasting seconds to minutes
severe intensity
electric shock, stabbing, shooting,sharp
precipitated by stimuli of moving mouth, talk eat, clean.

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58
Q

Trigeminal neuralgia Causes

A

Primary idiopathic.
relating to age
secondary: skull abnormality, malignancy, MS

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59
Q

Trigeminal neuralgia Management

A

MRI, to identify if other cause, tumour etc.
Carbamazepine or gabapentin, (anticonvulsants)
surgery, microvascular decompression via gamma knife

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60
Q

whatmakes you think of secondary headache

A

over 50 years old with a new headache, jaw claudication (GCA). fever stiff neck (meningitis) papillodema, raised ICP headache. previous cancers. weakness that persists after headache (encephalitis or malignancy) cognitive decline.
thunderclap pattern

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61
Q

What is thunderclap headache.

A

Headache that comes on rapidly. reaches maximum severity in seconds. nausea and vomiting
sudden onset, severe, N&V. due to SAH

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62
Q

what is management of suspected secondary headache

A

CT Scan to identify cause

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63
Q

what is chronic idoioathic cranial hypertension and how to treat it

A

Raised ICH headache for no reason other than obesity and drugs.
Usually female. Young 20s
treat with diuretics
Remember obese girl with leopard print top with her mum in hallamshire

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64
Q

types of stroke and commonest

A

Ischaemic, commonest
hemorrhagic
SAH

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65
Q

Stroke in ACA

A

gait ataxia. leg and trunk weakness and sensory loss. akinetic mutism. loss of bladder control (incontinence), Dysarthria

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66
Q

Stroke in MCA

A

Unilateral weakness and sensory loss. facial droop aphasia, dysphagia
hemianopia
commonest site for stroke

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67
Q

Stroke in PCA

A

Homonymous hemianopia with macular sparing
visual agnosia
prosopagnosia

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68
Q

Stroke in Brainstem

which artery supplies this

A

stroke in PCA and Basilar. total paralysis but cognitive function and sensory from eye intact. locked in syndrome. consciousness and cognition intact

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69
Q

Stroke in lenicular region

which artery supplies this

A

Internal capsule is MCA supplied

Full contralateral hemiplegia, dysarthia, dysphagia

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70
Q

risk factors for stroke

which ones are for hemorrhagic- the first 2

A 
Hypertension- largest
smoking
hyperlipidemia
DM
Family History
Obesity 
previous TIA
Heart Defects
Carotid stenosis and bruti
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71
Q

what are the causes of ischeamic stroke and where do they come from

A

Usually thromboemboli from Common carotid, internal carotid, vertebral and subclavian.
1 in 5 strokes of those under 40 is dissection

72
Q

causes of hemorrhagic stroke

A

severe hypo or hypertension
raised ICP
Polycythemia rubra vera

73
Q

Investigations for Stroke

A

CT/MRI,

can do ECG to see if there is a cause, AF?

74
Q

Ischaemic stroke management for the Clot.

A

within 4.5 hours: Thrombolytic therapy, Alteplase. ( +aspirin 24 Hrs, +LMWH, +further Investigations and prevention) (potential for stent retrieval - Endovascular Intervention)

After 4.5 hours: LMWH + Aspirin

75
Q

ischaemic stroke further investigations

A

ECG,
Carotid doppler
CXR- heart enlargement
bloods- look for anemia, vasculitis, Polycythemia

76
Q

Ischemic stroke further management for patient (prevention, conservative)

A

statins, better control of hypertension. diabetes, dual antiplatelet. if due to AF then give warfarin
surgery to remove carotid plaque (internal carotid endarterectomy
Conservative, Speech therapy, Occupational therapy, Physio
stop smoking and exercise
Swallowing assessment

77
Q

Intracranial hemorrhage management

A

control ABC,
Surgery, Remove haematoma, surgical clipping stop all risk factors, control hypertension no more than 20% change
Stop antiplatelets, anticoagulants. normalise INR
look for signs of conning like hydronephrosis

78
Q

SAH presentation

A

Thunderclap headache
sudden onset very severe, usually occipital
nausea and vomiting
lack of consciousness

79
Q

SAH Investigations

A

CT Scan diagnostic

Can do CSF analysis

80
Q

SAH complications

A

bleeding causes hydrocephalus

can lead to cerebral ischemia or rebleed cause death.

81
Q

signs of SAH

A

Neck stiffness, kernegs sign

focal neurological deficit

82
Q

Cause of SAH

A

ruptured berry aneurysm

83
Q

risk factors for SAH

A 
Smokers
alcohol 
hypertension 
post menopause
family history 
bleeding disorders
84
Q

Management for SAH

A

control hypertension 20%
Dexamethasone- swelling
nimodipine - CCB reduce spasm and ischemia

85
Q

what is a TIA

A

same as a stroke but the clot leaves on its own and symptoms clear within 24 hours

86
Q

specific TIA sign

A

Amaurosis fugax- dark curtain coming over eye

87
Q

causes of TIA

A

Thromboembolism from carotid or AF

88
Q

Investigations in TIA

A

Done IOT find cause of TIA

MRI, Carotid doppler, ECG

89
Q

Management of TIA

A

Avoiding risk of stroke
hypertension control, diabetes, statins, smoking, exercise, diet, dual antiplatelet
carotid endarterectomy

90
Q

tool used to see urgency of referring TIA patient

A 
ABCD2, predicts when next stroke will be and urgerncy to refer to specalist 
Age>65 1 
Blood pressure>140/90 1 
clinical 
unilateral weakness 2 
speech and no weakness 1
Diabetic 1
Duration of symptoms
less than 1 hour 1
more than hour 2  
if score more than 4 then see within 24 hours. all TIA to be seen in 7 days
91
Q

tool used to asses stroke risk in AF Patient

A 
CHADSVASC2
congestive heart failure 1
hypertension 1
age>75 1
diabetes 1
stroke or tia 2
vascular disease (prior MI, PVD) -1
age >65 1
sex -female 1
9/9= 15 % change of stroke per year
92
Q

Cardinal features of parkinsons

A

rigidity
resting tremor
bradykinesia - less blinking small writing little steps, shuffling gait

postural instability
Asymmetrical

93
Q

causes of parkinson’s disease

A 
idiopathic parkinson's disease, commonest
trauma 
drug induced 
encephalopathy
wilsons disease
94
Q

Pathophysiology of parkinson’s disease

A

Degeneration of substantia nigra dopaminergic receptors- cant activate basal ganglia

95
Q

investigations and diagnosis of parkinson’s disease

A

Clinical and history

DAT Scan- dopamine transporter scan confirmatory

96
Q

management of parkinsonism

A

counciling, MDT approach, physio, parkinsons nurse,

Levodopa (co-careldopa)

MOAD/CMT inhibitors (second line)
surgery- ablation to subthalamic nucleus
manage depression

97
Q

Complications of parkinsons

A 
Depression
dementia 
resistant to Ldopa
psychosis
autonomic features, constipation, ED
98
Q

what does a broad based gait indicate

what are other features of this disease

A 
Cerebellar disease,
intention tremor
normal tone
 DANISH
dysdiadochokinesis, dysmetria
ataxia
nystagmus 
intention tremor
scanning dysarthria/ slurred speech (jerky speech)
hypotonia/ hyporeflexia
99
Q

what signs would make you exclude a Parkinson’s diagnosis

A

Early dementia,
symmetry
early falls
early autonomic features, incontinence

these are suggestive of normal pressure hydrocephalus - Idiopathic CSF Build up which is drained surgically

100
Q

what are the features of an essential tremor

what are the causes, investigations and treatment of this

A

no little rest tremor
no increased tone or dyskinesia
postural and action tremor
Structural abnormality, CT and Physio and B blockers

101
Q

what is huntington’s disease

A

Neurodegenerative disease caused by malfunction in huntingtin gene. causes neuronal cell atrophy.

102
Q

Pathophysiology and progression of huntington’s

A

Starts of with increased dopamine production and atrophy of the indirect pathway. this causes less inhibition and the huntingtons cardinal signs (chorea and Hyperkinesia).
as huntington’s progresses, the direct BG pathway is lost leaving only the inhibitory function of the basal ganglia to be active, causing hypokinesia
atrophy of the brain also causes psychiatric problems.

103
Q

Presentation of huntington’s

A

Cardinal- Chorea- hyperkinesia
dementia
psychiatric problems/ personality change
other signs: abnormal eye movements, chorea, ataxia, rigidity (late sign), eventually develops to parkinsonism signs

104
Q

Diagnosis of huntington’s via genetic screening

A

36 CAG triplet repeats

105
Q

Huntington’s genetic features

A

Autosomal dominant
100% penetrance,
gets more and more repreats with every generation - starting earlier (anticipation)

106
Q

Huntington’s treatment

A

Neuroleptics- Dopamine receptor blockers, (promazine Hydrochloride)
depression- SSRIs, Sertraline
family screening
MDT, Physio, Occupational Health, Huntington’s nurse, social care

107
Q

what is Multiple Sclerosis

A

Chronic Inflammatory demyelinating disease of the CNS

108
Q

Prevalence of MS

average age of onset

A

commonest cause of neurological deficiency in adults
average onset 20-40 Y O
0.1% of population in UK

109
Q

Risk Factors and of MS

A 
Risk increases the further you get from the equator
being female
vit D deficiency 
family history
sanitation 
diet
race, commoner in caucasian and white
110
Q

Pathophysiology of MS

A

demyelination plaques due to T cell mediated inflammation. plaques most commonly in optic and periventricular regions.
as inflammation occurs, relapse. as it subsides, remyelination it remittes

111
Q

What are the different patterns of presentation of MS

A

Relapsing remitting, 80% most common
Primary Progression
secondary progression- starts relapsing remiting and becomes progressive
begine, only has a few episodes

112
Q

Presenation of MS

what are common symptoms and a MS specific Sign

A

like a stroke, but gets better then worst again, can happen anywhere in CNS, optic, spine, cerebellum, brainstem
Epilepsy and trigeminal neurlagia are common
can cause depression or dementia
+ve Uhthoffs phenomenon

113
Q

Differential diagnosis Of MS

A

on first presenation could be stroke, Betchets disease

SLE (look for extremly +ve family history)

114
Q

what is uhthoff’s phenomenon

A

MS patients symptoms get worst after putting them in a hot bath, due to heat slowing down conduction

115
Q

Diagnostic criteria for MS

Mcdonald’s diagnosis

A

needs to have 2 or more episodes that are disseminated in time, and disseminated in lesion space
exclude all other causes

116
Q

Investigations for MS

A

MRI- tries to identify demyelinating plaque or exclude other causes
CSF analysis - shows inflammatory markers in CSF
No inflammation in bloods

117
Q

Management of MS

A

Conservative: Physio, OH, Neurologist, MS Nurse speech, counciling, psychological counseling.
education on lowering stress and uhthoff’s.
symptoms elevated by coolness
Tremor treated by B blockers
SSRI sertraline, for depression

Disease modifying treatment is IV methylprednisolone steroids.
prevention of onset, B Interferons.
Immunosuppression and monoclonal antibodies

118
Q

what is meningitis

A

Inflammation of the meningies

119
Q

What are the causes of meningitis,

A

Viral, Bacterial, fungal or parasite
most common Streptococcus pneumoniae
less common but also prevalent: niesseria meningitidis

Paraneoplasia, meningioma, Drug Induced, Autoimmune (SLE)

120
Q

Which meningies are affected in meningitis

A

Pia and Arachnoid

121
Q

Presentation of meningitis

A

Triad:
Pyrexia,
Neck Stiffness
Headache

other: Photophobia, vomiting, malaise, rigiors
can develop into sepsis
loss of consciousness, focal seizures

122
Q

Signs of meiningitis

A

petechial rash
Kernig’s sign- flex hip and knee then extend knee, pain= Kernig’s sign +ve
Brudzinski signs- knee and hip flex spontaneously when neck is flexed

123
Q

What else causes Kernig’s signs and Neck stiffness

A

SAH

124
Q

management for meningitis pre hospital

A

IM/IV Benzylpenicillin

125
Q

Management for Meningitis

A

IV Cefotaxime (+Ampicillin if over 55)
Steroids, IV Dexamethasone
Investigate further
asses sepsis

126
Q

Investigations and Diagnosis for meningitis

A 
Bloods ESR CRP
Definitive: lumbar Puncture, CSF MS & C 
if gram +Ve, strep pneumoniae
gram -VE, neisseria meningitidis (notifiable)
CXR TB
LP is CI in raised ICP or Pectinal rash
127
Q

Who’s at risk of meningitis

A

Students travelers

immunocompromised

128
Q

what is the causing agent of Encephalitis

A

Herpes simplex, commonest cause
other:
Herpes zoster, HIV Measles and Mumps

129
Q

Presentation of encephalitis

A

History of general unwell, flu like symptoms

day of presentation= altered GCS Fever Seizures Confusion memory loss

130
Q

Investigation of Encephalitis

A

MRI exclude other
EEG- diagnostic
blood cultures and lumbar puncture MC&S to identify cause

131
Q

Treatment of Encephalitis

A

Treat causative agent,

Antiviral, IV acyclovir

132
Q

what are the different kinds of seizures

A

Partial/ focal- can be simple or complex ( consciousness)
partial can develop into generalised, secondary generalised
primary generalised - can have absent, myoclonic (isolated jerky movement) that develops into tonic clonic

133
Q

what are preictal features

A

symptoms that occur before seizure, general feeling or auras, jamis vue, deja vu. commonly occurs before focal seizure (Temporal lobe)

134
Q

what are Post ictal features and what are they indicative off.

A

Can have weakness, (todd’s palsy) resolves after a while, aphasia, dysphasia. these are signs of focal seizure ( Frontal lobe)

135
Q

features of frontal lobe epileptic features

A

Partial seizure, consciousness retained, enter jacksonian march or seizure, where they are fully aware of what they are doing but have no control.
develops todd’s palsy afterwards, Hemiparesis that resolves within 2 days

136
Q

Features of a temporal lobe epileptic seizure

A

partial seizure, can be conscious or unconscious. gets automatism complex, (start doing things automatically) no memory retained. dysphasia, lip smacking, de ja vu jamai vue. usually tend to have isolated muscle seizures. move only one limb.
can develop into secondary generalised seizure.
has features afterwards, or other post ictal features

137
Q

Features of a generalised seizure

A

can start of with myoclonic isolated muscle movements, can start of as partial then develop. develops into tonic clonic seizure.

138
Q

Length of seizures,

A

30 seconds -120 seconds. generally under 3 minutes

139
Q

examination a=of a seizure, things you can ask witness

A

How long did the seizure last
what was the character of the seizure, how did it change, phases of the seizure. the speed of convulsions.
if incontinence.
Sequence of events of seizure.
any post ictal signs they have noticed like dysphasia

140
Q

Examination of a seizure, what would you ask the patient

A

what were you doing before seizure
did you notice any preictal symptoms, deja vu jamais vu, auras, general feeling.
did you retain consciousness during the seizure. do you have monory of what happened
post ictal features, dysphasia, todd’s Palsy.
does their tongue hurt, indication of tongue biting.
incontinence during seizure

141
Q

Investigations of a seizure

A 
any seizure needs to have CT/MRI
witness statement 
EEG
also try to exclude other causes, ECG, BP, Hypoxia, Pseudoseizure due to stress. 
CXR, TB, Sarcoidosis, SLE. 
Electrolytes
142
Q

commonest cause of seizures

A

2/3. Idiopathic generalised epilepsy, usually familial.

143
Q

other causes of seizures

A

pseudoseizure - stress related
Focal epilepsy, (secondary) due to anything pressing on brain, Tumour. SAH, Meningitis
metabolic- low or high Na, low glucose, Low Ca, Uremia.
Low BP, syncope. heart problems
TB, Sarcoidosis, SLE

144
Q

Management of seizures

conservative

A

education on potential triggers, alcohol, substance, stress. medications
education on maintaining safety, driving. avoid baths, locking doors.

145
Q

Pharmacological management of seizures

A

antiepileptic drugs- carbamazepine - for tonic clonic, and partial seizures
sodium valproate- for all other kinds

146
Q

Surgical management of seizures

A

Vagus nerve stimulation,
surgical- hippocampal section if sclerosis
corpus callosum section

147
Q

Prognosis of epilepsy

A

majority are seizure free 2 years after starting meds

148
Q

what is the blood supply if the spinal cord

A

Vertebral arteries- anterior spinal artery
Intercostal arteries
lumbar vessels

149
Q

spinal cord landmarks

A

from medulla till L1/2 then conus medullaris and it extends as cauda equina

150
Q

what are the principle features of spinal cord compression

A

spastic hemiparesis, or tetra or quadra. (weakness and stiffness)
radicular pain at level of compression (pain radiating along nerve root
sensory loss below compression
if compression above S234 causes retention and constipation ( detrusor and sphincter contract at the same time

151
Q

what are the causes of spinal cord compression

A

spinal neoplasm
Disc and vertebral lesions (trauma, osteoporotic fracture
TB- Pott’s disease
epidural hemorrhage or hematoma

152
Q

What are the spinal cord neoplasms

A

Extradural- metastatic
Extrameduallary- meningioma
Intramedullary- glioma

153
Q

Investigations for spinal cord compression

A

Gold standard is MRI

Investigate other causes

154
Q

managment for spinal cord compression

A

surgical decompression, removal of tumour.

if malignant then chemo+radiotherapy

155
Q

what is cauda equina syndrome

A

cord compression between L2 and S5

156
Q

causes of cauda equina syndrome

A

same as SP compression. common iatrogenic from LP. (epidural hematoma) this is why LP is CI in raised ICP

157
Q

presentation of cauda equina syndrome

A

saddle anesthesia, severe back pain, incontinence, sciatica, gait disturbance

158
Q

Management of cauda equina syndrome

A

laminectomy- remove vertebra to allow for decompression.

159
Q

causes of CN 7 palsy

A 
Idiopathic Bell's palsy 70%
ramsay hunt syndrome- herpes zoster
Lyme disease 
meningitis 
stroke
tumour 
MS
Diabetes 
Parotid tumour
160
Q

CN7 Palsy presnetaion

A

Unilateral facial weakness, speech difficulty,
no taste in ant 2/3 of tongue
sound hypersensitivity due to stapedius not working.

161
Q

risks and associations with Bell’s palsy

A

unknown onset during the night,
increased risk in pregnancy
diabetes

162
Q

Investigations and diagnosis of bells palsy

A

Exclude other causes. MRI, cultures serology for lyme and ramsay hunt

163
Q

Management of bells palsy

A

if present within 3 days. prednisone
if afterwards corticosteroids.
potential surgery to close eyelid

164
Q

Prognosis of Bell’s palsy

A

if paresis most recover in a few weeks

if plegia, 80% recovery

165
Q

what is the commonest neuropathy

A

Sensory motor chronic neuropathy due to DM

166
Q

What is a sign of brain tumour

A

Papilloedema

167
Q

What are neuroleptics, what do they cause and when do you use them

A

antipsychotic class, used in huntington’s sice dopamine antagonist (levomePROMAZINE)

cause drug induced parkinson’s

168
Q

Treatment for essential tremor

A

Physio and B blockers

169
Q

Subdural hemorrhage Presentation

A 
Altering consciousness and GCS
Physical or intellectual slowin
Sleepiness
headache
personality changes
170
Q

Subdural hemorrhage cause

A

Most are from trauma a while ago, minor trauma

can occur with falls in epileptics r alcoholics
elderly are susceptible

171
Q

Subdural hemorrhage Investigations

A

CT / MRI showing clot or midline shift (Crescent shaped)

172
Q

Subdural hemorrhage Management

A

1st line: irrigation/evacuation Blurr twist

2nd: craniotomy

173
Q

Signs of Subdural hemorrhage

A

Increased ICP
Seizures
focal neurological features

174
Q

Extradural haemorrhage cause and pathophysiology

A

often occurs after immense trauma causing fracture of temporal or parietal bone causing a Laceration in meningeal artery
or trauma leading to a tear in venous sinus

175
Q

Extradural haemorrhage Presentation

A

Deteriorating consciousness after head injury

Initially not producing anything but gets worse progressively
few hours later ICP rises
Vomiting headache
Low GCS
Seizures
Hemiparesis plus brisk reflex (hyperreflexia)
Ipsilateral pupil dilates
progresses to bilateral weakness
Breathing difficulty (due to compression)

176
Q

Investigations of extradural Haemorrage

A

CT Shows haematoma, lens shaped, more rounded

X ray may show fracture

177
Q

Management of Extradural haemkrrage

A

Stabilize and transfer to neurosurgery for clot evacuation
Airway care
Mannitol to reduce ICP

Hayders Phase 2A (10 decks)

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