New Neurology Flashcards

1
Q

What is presbycusis?

A

Age related sensorineural hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Otosclerosis?

A

autosomal dominant replacement of normal bone with spongy vascular bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is menieres disease?

A

Recurrent episodes of vertigo, tinnitus and sensorineural hearing loss, lasting mins-hours. Vertigo main complaint!

Middle aged adults
Feeling of aural fullness/pressure
Nystagmus/positive romberg test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations in Meniere’s disease

A

Menieres triad
- Otoscopy - Normal ear drum
- Audiometry - Sensorineural hearing loss
- Tympanometry - normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pharmacological mx of menieres

A

Prochlorperazine (acute vertigo and nausea) [Acute attacks]
Betahistine medication (H1 agonist that acts as a Vestibular sedative) [Prevention]
Intratympanic gentamicin injection if surgical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Acoustic Neuroma?

A

AKA vestibular schwanomma. Tumour arising from schwann cells myelinating CN8. Usually presents between 40-60yo.

Associated with type 2 neurofibromatosis

Presents similar to menieres (vertigo, tinnitus, S hearing loss) BUT also has absent corneal reflex and possible facial paralysis

Affected cranial nerves:
- Men. symptoms (VIII)
- Absent corneal reflex (V)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can acoustic neuroma present?

A

Depends on cranial nerves affected
- CN5: Absent corneal relfex
- CN7: Facial palsy
- CN8: Unilateral sensorineural hearing loss and tinnitus, vertigo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ix of Acoustic Neuroma

A

Audiogram and examination show sensorineural hearing loss.

MRI Gold standard imaging for diagnosis and tumour tracking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mx and comps of acoustic neuroma

A

Conservative or
Tumour excision or
Radiotherapy
Permanent hearing loss (CN8), permanent facial weakness (CN7)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is an essential tremor, give features and management?

A

Autosomal dominant condition usually affecting both arms.

Postural tremor: worse when arms stretched out
Improved by alcohol and rest
Most common cause of titubation (head tremor)
Managed with propanolol, or primidone second line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define Extradural Haemorrhage with its main cause and epidemiology

A

Cranial bleeding above the dura mater.

Usually caused by trauma to pterion of skull, causing rupture of middle meningeal artery in temporo-parietal region. Can associate with temporal bone fracture.

Usually found in young adults

Blood doesnt cross suture lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why can extradural stroke present slowly at first before becoming more severe?

A

If bleeding is slow, symptom onset is slower (lucid interval) before there is a sudden, rapid decline when intracranial pressure increases enough to compress brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe non contrast ct appearance in extradural haemorrhage (3)

A

Biconvex, hyperdense haematoma
Blood doesnt cross suture lines
Shows midline shift (increased pressure can cause cause brain shifting/herniation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 main herniation complications of haemorrhagic stroke?

A

Supratentorial herniation (cerebrum against skull, compressing arteries and causing ischaemic stroke)

Infratentorial herniation (Cerebellum pushed against brainstem, compressing area that controls consciousness, respiration, heart rate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cushings triad and how is it treated?

A

Body’s response to increased intracranial pressure, signifies severe lack of oxygen in brain tissue
- Bradycardia
- Irregular respirations
- Widened pulse pressures (increased systolic, decreased diastolic)

Treated with IV mannitol to reduce ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define Subdural haemorrhage with its main cause and epidemiology

A

Bleeding below dura mater, caused by bridging vein rupture.

Usually occur in elderly/alcoholic patients but can occur in babies (shaken baby syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

causes of bridging vein rupture

A

Brain atrophy; with age. Stretches bridging veins, meaning they stretch over gaps unsupported.
Alcohol abuse: Causes walls of vein to thin
Trauma
Falls
Shaken baby syndrome
Acceleration/deceleration injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

non contrast ct appearance of subdural haemorrhage

A

Bleeding between the dura mater and arachnoid
- Follows contours of brain and crosses suture lines, forming a crescent shape

Acute (hyperdense mass)
Chronic (Hypodense mass)
Acute on Chronic (both)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what gcs requires intubation

A

8 or below

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

specific surgery in subdural haemorrhage

A

Burrhole washout if haemorrhage small

Craniotomy if large haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

define subarachnoid haemorrhage with main cause

A

Bleeding below the arachnoid layer, where CSF is located.

Main cause is a ruptured saccular (or Berry) aneurysm, with majority located between anterior communicating artery and anterior cerebral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

RF for subarachnoid haemorrhage (7)

A

PKD (Associated with berry aneurysm)
Connective tissue disorders (Ehlers-Danlos, Marfans)
Family history
Increasing age
HTN
Smoking
Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

typical presentation of subarachnoid haemorrhage

A

Sudden onset occipital “thunderclap” headache, following strenuous activity, with associated neck stiffness and photophobia. Smaller, “Sentinel” headache may have preceded thunderclap

Black, female, 45-70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

signs/symptoms of subarachnoid haemorrhage

A

Thunderclap headache
Meningism (Headache, photophobia + neck stiffness)
Fixed dilated pupil (third nerve palsy - especially in posterior communicating artery rupture)
6th nerve palsy
Kernigs and Brudzinskis due to meningism also
Nausea/vomiting, weakness, confusion, coma, reduced consciousness, speech reduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
ix of subarachnoid haemorrhage
Urgent non contrast CT head (blood in subarachnoid space/basal cisterns) CT angiography to locate bleed source ECG to detect arrhythmia/abnormality If CT non conclusive, - Lumbar puncture (RBCs in CSF and Xanthochromia) 12 hours after onset.
26
Define Kernig's and Brudzinski's signs
Kernig - Inability to straighten bent leg without pain when hip flexed to 90 degrees Brudzinski - Passive flexion of neck in supine patient elicits hip and knee flexion Suggest meningitis/meningism
27
ct appearance in subarachnoid haemorrhage
Blood in subarachnoid space (hyperdense) - Star shaped lesion (Blood filling in gyro pattern)
28
Mx of subarachnoid haemorrhage
Surgical 1st/GOLD - Endovascular coiling (clipping also possible but more complications) Nimodipine to prevent vasopasms IV Mannitol to reduce ICP Sodium valproate for seizures
29
Define meningitis
Inflammation of the meninges (specifically leptomeninges - pia and arachnoid). Can be due to viral, bacterial or fungal cause. Notifiable disease
30
Viral Causes of meningitis
More common but less severe - Coxsackie virus - HSV (Herpes simplex virus) - Varicella Zoster virus - Mumps
31
bacterial causes of meningitis
Most common - S. pneumoniae and N. meningitidis Children - ^ and H influenzae Elderly and pregnant - Listeria Monocytogenes (pregnant avoid cheese) Newborns - ^ and Group B strep
32
How do n meningitidis, s pneumoniae, group b strep and listeria monocytogenes present on gram film?
N meningitidis - Gram negative diplococci (Only one that causes non blanching rash!) S pneumoniae/Group B strep - Gram positive cocci in chains Listeria monocytogenes - Gram positive bacillus
33
signs/symptoms of meningitis
Signs - Neck stiffness, headache, photophobia (avoids light) - Phonophobia (avoid sound) - Papilloedema (optic disk swelling) - Kernig sign - Brudzinski sign - Non blanching rash (N meningitidis only) Pyrexia, reduced GCS
34
ix of meningitis
Blood culture 1st line - Bacterial or negative for viral Lumbar puncture GOLD Bacterial - Cloudy/yellow - Protein high - Glucose low (<50% normal) - WCC high (Neutrophil) Viral - Clear appearance - Protein small raise/normal - Glucose normal (>60% normal) - WCC high (lymphocytes) (Gram stain identifies bacteria and CSF PCR identifies viruses)
35
fungal appearance of csf in meningitis
Cloudy and fibrous Protein high Glucose low WCC high - Lymphocytes!
36
mx of bacterial meningitis
Primary care: Immediate IV or IM benzylpenicillin (if suspected meningococcal) and hospital referral Hospital - Dexamethasone (steroid) - Cefotaxime or Ceftriaxone IV Give Amoxicillin if under 3 months or over 50 to cover listeria Contact tracing and single dose oral ciprofloxacin for contacts
37
comps of meningitis
Hearing loss Seizures Cognitive impairment Hydrocephalus Sepsis
38
Upper motor neurone lesion signs vs lower motor neurone lesion signs Type of paralysis -reflexia Fasciculations Babinski sign Voluntary movement Muscle tone and power
UMN Spastic paralysis Hyperreflexia No fasciculations Babinski positive Voluntary movement slowed Muscle tone and power kept LMN Flaccid paralysis Hyporeflexia Fasciculations Babinski negative Voluntary movement gone Muscle tone and power lost (babinski - toes curl up when bottom of foot is stroked fasiculations - brief spontaneous contractions under skin)
39
define ms
Type 4 hypersensitivity reaction in which there is autoimmune attack against oligodendrocytes (which create myelin) in the CNS (Brain/Spinal cord). Causes plaques of demyelination. Lesions vary, meaning plaques are “disseminated in space and time” - affect different areas of CNS at different times/ events.
40
disease progression in ms
Relapsing remitting (most common) - Episodic flare ups without full recovery in between, meaning flares worsen over time. (Most common and often progress to secondary progressive) Secondary progressive - Symptoms start getting worse without remission Primary progressive - Symptoms worsen without remission (/) Progressive relapsing - Constant attack with superimposed flare ups
41
what is uhtoffs phenomenon?
Symptoms worsen with heat (e.g. hot bath) or exercise. New myelin is inefficient, and doesn’t tolerate temperature rise effectively.
42
what triad is associated with ms?
Charcot’s neurological triad - Nystagmus (involuntary side-to-side/up-down rapid eye movements) - Dysarthria (slowed, slurred speech) - Intention tremor
43
signs/symptoms of ms
Optic neuritis usually first (Loss of vision, eye pain, pale optic disk, double vision) Internuclear ophthalmoplegia (eye muscle paralysis which impairs lateral gaze) Lhermitte’s sign - Electric shock sensation when flexing neck UPPER motor neurone signs Bowel, bladder, erectile dysfunction Ataxia Sensation loss (Uhthoff’s and Charcot’s neurological triad already mentioned)
44
what criteria is used in diagnosis of ms?
McDonald criteria (think McDonald’s M!) - 2 or more relapses with evidence of 2 or more lesions, or one lesion with reasonable history of relapse
45
ix in ms (3)
MRI Brain/Spine - Demyelinating plaques (new enhance with contrast, old don’t - showing dissemination in space and time) Lumbar puncture - Oligoclonal IgG bands in CSF Visual evoked potential studies (responses to visual stimulus) - Shows delayed nerve conduction
46
mx of ms
During acute relapse - Oral/IV methylprednisolone first, cladribine - Plasma exchange Maintenance - Interferon beta - IV monoclonal antibodies Cladribine second line in ongoing secondary progressive but causes cancer and is teratogenic
47
comps of ms and there managements (3)
Spasticity - Baclofen and gabapentin Neuropathic pain/depression - amitriptyline Physiotherapy for Spasticity and mobility impairment
48
what are some disease modifying durgs in ms with their indications?
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided) IV Natalizumab - monoclonal antibody IV Ocrelizumab Oral fingolimod SC beta interferon SC Glatiramer acetate
49
what is huntingtons?
Autosomal dominant trinucleotide repeat disorder, which causes deterioration of nervous system and an excess of dopamine. Also known as Huntington’s chorea (Chorea= involuntary jerky movements) HTT gene on chromosome 4 - Mutated Huntingtin proteins aggregate in neuronal cells of caudate and putamen. Causes cell death of GABAergic and cholinergic neruones, causing ACh and GABA deficiency, so less dopamine inhibition. Excess dopamine causes excess movement. Genetic anticipation - The more copies of the protein DNA polymerase adds on in the sperm, the earlier onset and more severe the disease
50
signs and symptoms of huntingtons?
Usually asymptomatic until 30-50 years Prodromal - Irritability, depression, cognitive problems Chorea - Jerky involuntary movements Eye movement disorders Dysphagia/dysarthria Dementia, seizures, death within 15 years
51
ix in huntingtons
Clinical diagnosis - Genetic testing GOLD CT/MRI - Caudate and striatal atrophy - increased size of lateral ventricles
52
other causes of chorea
Hyperthyroid Wilson’s SLE Dementia
53
mx of huntingtons
Uncurable Chorea - Diazepam and tetrabenazine (Benzodiazepine and dopamine depleting agent)
54
define parkinsons disease
Neurodegenerative movement disorder characterised by loss of dopaminergic neurones in Substantia Nigra Pars Compacta of basal ganglia. Misfolded a synuclein proteins called Lewy bodies also present histologically (dark eosinophilic inclusions) Causes a dopamine deficiency
55
what are the parkinsonism symptoms
Resting Tremor Bradykinesia Rigidity Postural instability
56
signs and symptoms of parkinsons (other than parkinsonisms)
Resting tremor Cogwheel rigidity Shuffling gait Reduced arm swing Non motor: Loss of smell Sleep disturbance Depression, anxiety Dementia
57
ix in parkinsons
Clinical diagnosis - bradykinesia and 1 other Parkinsonism sign (Bradykinesia = slow, difficult movements. Smaller handwriting, shuffling gait, reduced arm swing etc) Dopamine agent trial shows improvement
58
mx of parkinsons
If Severe: Levodopa + Decarboxylase inhibitor (boost dopamine and Di prevents L-dopa breakdown) - Co-careldopa (Levodopa and carbidopa) Otherwise: Dopamine agonist - Ropinirole Monoamine oxidase B inhibitor (MAOBi) (stop breakdown of circulating dopamine) - Selegiline
59
comps of parkinsons
Disease progression and motor fluctuations (off periods when treatment stops working) - Freezing (sudden stop of movement) - Dyskinesia - Dementia
60
differentials of parkinsonisms
Benign Essential Tremor Wilson’s disease Encephalitis causing degeneration of substantia nigra Trauma
61
define myasthenia gravis
Type 2 hypersensitivity reaction causing autoimmune destruction of the post synaptic membrane at the neuromuscular junction of skeletal muscle. Antibodies to acetylcholine receptors in 85% of cases. (Anti-AChR) 2x in women. Mostly affects facial muscles. Strong association with thymoma/ thymic hyperplasia
62
signs/symptoms of myasthenia gravis (6)
Mostly affects proximal and small muscles of head and neck - Muscle weakness with fatigability, worse with exertion better with rest (e.g. patient counting to 50 will struggle in later numbers) - Ptosis (eyelid droop) and diplopia (double vision) - Jaw weakness and weak swallow (dysphagia) - Head drop - Facial paresis and slurred speech - Snarl when attempting to smile (myasthenic snarl)
63
how to check for muscle fatigability on examination (3) and what should you check? (myasthenia)
Repeated blinking causing ptosis Counting to 50, speech becomes slurred and quieter towards end Repeated abduction of one arm will result in weakness in said arm compared to other Forced Vital Capacity should also be checked
64
ix in myasthenia gravis?
Antibodies - AchR antibodies (anti-MuSK and anti-LRP4 less sensitive) - Anti-MUSK - Anti LRP4 CT thorax - look for thymus growth/thymoma (rule out) Tensilon test - Used to be done but causes arrhythmia so dont even think about it
65
drugs that exacerbate MG muscle fatigability
penicillamine quinidine, procainamide beta-blockers lithium phenytoin antibiotics: gentamicin, macrolides, quinolones, tetracyclines Most common factor is exertion!
66
mx of myasthenia gravis
Long acting acetylcholinesterase inhibitor - Pyridostigmine first line Immunosuppression (not started at diagnosis, usually started later) - Prednisolone Thymectomy may be needed (as many patients also have thymic hyperplasia)
67
myasthenia gravis brief pathophysiology
Unexplained destruction of Only UMNs and LMNs. - No effect on sensory neurones (distinguishing point from MS etc) - No effect on eyes (distinguishing from myasthenia gravis) - No cerebellar involvement - SOD1 mutation association in ALS
68
Define guillain barre syndrome with causes
Acute autoimmune demyelination of the peripheral nervous system, following an upper resp tract or GI infection (e.g. gastroenteritis) Acute, symmetrical, ascending weakness! Can be caused by: Bacteria: - Campylobacter Jejuni - M. pneumoniae Viral: - Cytomegalovirus - EBV
69
guillaine barre disease course (4)
Initial GI or URT infection Symptoms start after 2 weeks Symptoms peak 2-4 weeks further Recovery period of months to years
70
pathophysiology of guillain barre syndrome
Molecular mimicry. Pathogenic antigens resemble Schwan cell proteins so when immune response is launched, there is also destruction of myelin sheath. Demyelination occurs in patches down length of axon (segmental demyelination). Schwann cells can remyelinate so patients recover over time. Affects sensory and motor nerves.
71
signs and symptoms of guillain barre syndrome
Symptom onset 2-3 weeks after preceding infection. Proximal muscles affected first Symmetrical ascending weakness beginning in legs/feet. Areflexia Reduced sensation Paraesthesia Sensory loss Respiratory distress if lungs affected Autonomic dysfunction (bowel/bladder, sweating, raised BP/pulse, arrhythmia)
72
ix of guillain barre syndrome
Brighton criteria used to make clinical diagnosis, can be supported by: - Nerve conduction studies (reduced conduction) - Lumbar puncture (high protein in CSF, normal cell count and glucose) Antibodies: subtype of GBS AIDP (90%) - Anti ganglioside Miller fisher syndrome (eyes affected first) - anti GQ1b Do spirometry to assess risk of resp failure
73
mx of guillain barre syndrome (2 tx + 2 complication tx)
IV immunoglobulin 5 days (CI if IgA deficiency) Plasma exchange VTE Prophylaxis (LMWH) Ventilation if low FVC
74
umn lesion area
anywhere from pre central gyrus to anterior spinal cord
75
lmn lesion area
anwhere from anterior spinal cord to innervated muscle
76
how is muscle power affected in umn lesions?
In arms flexors>extensors In legs extensors>flexors
77
types of mnd
Amyotrophic lateral sclerosis (50% of patients) typically LMN signs in arms and UMN signs in legs in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase Primary lateral sclerosis UMN signs only Progressive muscular atrophy LMN signs only affects distal muscles before proximal carries best prognosis Progressive bulbar palsy palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei carries worst prognosis
78
presentation of mnd
asymmetric limb weakness is the most common presentation of ALS the mixture of lower motor neuron and upper motor neuron signs wasting of the small hand muscles/tibialis anterior is common fasciculations the absence of sensory signs/symptoms vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory
79
mx of mnd (2) what is prognosis?
Riluzole (protects neurones from glutamate induced damage) Respiratory support (non invasive at home) 50% die in 3 years
80
gene associations with alzheimers?
APoE e4 - APoE usually helps break down beta amyloid but e4 version less effective. Down’s (Trisomy 21) - Increased APP (amyloid precursor protein) production (APP gene also on C21). APP broken down incorrectly becomes beta amyloid. PSEN1, PSEN2
81
key histological findings in alzheimers
Senile plaques of beta amyloid proteins (APP incorrectly broken down into sticky, insoluble b amyloid) (extracellular) Neurofibrillary tangles of hyperphosphorylated tau proteins (intracellular)
82
signs/symptoms of alzheimers (4)
Insidious onset and slow progressive decline Poor memory (short term early, long term late) Speech problems (receptive and expressive dysphagia) Loss of executive function (planning/problem solving) Disorientation/lack of recognition of places, people or objects
83
how would alzheimers affect behaviour? (4)
Emotional instability Depression/anxiety Withdrawal/apathy Disinhibition (Socially/sexually inappropriate behaviour)
84
how would alzheimers affect daily living? (3)
Loss of independence Early on loss of higher level function (finances, difficulties working) Later loss of basic function (washing, eating, walking)
85
how is alzheimers diagnosed?
Based on DSM-V criteria and MMSE (Mini mental state examination) (25+ normal, <17 severely impaired) MRI - Generalised brain atrophy with medial temporal then later parietal predominance Brain biopsy is GOLD but can only be done after death
86
Mx of alzheimers
Supportive: Improve cognitive function - Exercise - Music - Board games - Cognitive stimulation program ACh-esterase inhibitor (Donepezil) NMDA receptor antagonist (Memantine)
87
Define Vascular dementia
Dementia caused by cerebrovascular damage causing hypoperfusion of neuronal cells. Presents in patients with Stroke/TIA history, UMN signs and general condition decline. Shows a stepwise decline with symptoms worsening after each cerebrovascular event.
88
Investigations and treatment of vascular dementia
Mini mental state exam CT/MRI of brain - Multiple cortical and subcortical infarcts - Atrophy of brain cortex Treated with management of risk factors (lower BP, cholesterol, diabetes etc)
89
define lewy body dementia
Dementia with Parkinsonism (Resting tremor, bradykinesia, rigidity, postural instability). Alpha synuclein misfolds in neurones and aggregates to form Lewy Bodies, which deposit in cortex and substantia nigra causing neuron death.
90
sx of lewy body dementia
Presents with dementia symptoms first (memory, focus, speech, understanding issues) Parkinsonism develops later Sleep disorders like sleep walking/talking, and hallucinations are also very common in LBD If Parkinsons first, it is Parkinson Dementia
91
mx of lewy body dementia
Dopamine analogue - Levodopa ACh-esterase inhibitor - Donepezil
92
Define fronto temporal dementia
Focal degeneration of frontal and temporal lobes. Pick’s disease is most common type. Loss of over 70% of spindle neurones. Frontotemporal dementia (Pick’s disease) Progressive non fluent aphasia (Chronic progressive aphasia) Semantic dementia
93
common features of frontotemporal lobar dementias
Onset before 65 Insidious onset Relatively preserved memory and visuospatial skills
94
What is Pick’s disease, how does it present and what macroscopic and microscopic changes are found
AKA Frontotemporal dementia. Personality change and impaired social conduct! Hyperorality, disinhibition, increased appetite, perserveration beahviours. Focal gyral atrophy with knife-blade appearance Macro - Atrophy of frontal and temporal lobes Micro - Pick bodies - spherical aggregations of tau protein (silver staining) - Gliosis - Senile plaques and neurofibrillary tangles
95
What is cpa? (chronic progressive aphasia?
Clues in the name. Short utterances that are agrammatic. Comprehension preserved
96
what is semantic dementia?
Fluent progressive aphasia. Speech fluent but empty, not much meaning. Memory better for recent rather than remote events
97
what are pick bodies?
3R isoform of tau proteins These become hyperphosphorylated and form tangles, causing atrophy in frontoteporal lobes (In alzheimers, the isoform is 3R+4R)
98
Give primary and secondary causes of headache
Primary - Migraine - Tension - Cluster Secondary (to other pathology) - GCA - Cerebrovascular disease - Subarachnoid haemorrhage - Truma
99
define migraine
Episodes of recurrent, unilateral throbbing headache. May or may not have an aura and often has visual changes (e.g. photophobia, diplopia etc). Can last up to 72 hours, and classically preceded by an aura - Visual, progressive, lasting 5-60 minutes.
100
Common migraine triggers
CHOCOLATE Chocolate Hangover Orgasms Cheese Oral contraceptive Lie ins (tiredness) Alcohol Tumult (loud noise) Exercise
101
Signs/symptoms of typical/atypical aura
Typical: Lasts 5-60 mins and fully reversible. - Visual changes (zigzag lines, distortion etc) - Smell changes - Paraesthesia Atypical: >60 mins - Diplopia - Motor weakness (hemiplegic migraine!) - Poor balance - Reduced consciousness
102
Ix in migraine
Clinical diagnosis: Migraine with/without aura (at least 2/4 symptoms, 1 associated symptom, no attribution to another disorder) CT/MRI to exclude secondary haemorrhage ESR exclude GCA
103
tx of migraine
Acute prevention - Oral Sumatriptan (5-HT receptor agonist (mimic serotonin)) with/without aspirin Prophylaxis - Propanolol - Amitriptyline - Topirimate (antiemetic) AVOID Opiates
104
define tension headache
Most common type of headache. Bilateral “pressing/tight” headache. Lasts minutes to hours. No associated symptoms except photo OR phonophobia
105
Define cluster headache
Severe, unilateral periorbital headache, with associated autonomic features, affecting same side face/eyes. Lasts 15-180 mins. AKA Trigeminal Autonomic Cephalalgia
106
Signs/symptoms of cluster headache
Severe unilateral, periorbital, crescendo headache, lasting 15mins to 3 hours. Clusters of headaches, (Boring/hot poker pain “worst pain ever”) Ipsilateral autonomic symptoms - Ptosis (eyelid droop) - Miosis (excessive constriction of pupil of eye) - Teary, bloodshot eye - Nasal congestion/rhinorrhoea
107
diagnosis and mx of cluster headache
Clinical diagnosis (5+ similar headaches) Acute - Triptans - High flow oxygen (AVOID paracetamol, NSAID, Opioids) Prophylaxis - Verapamil (CCB) - Prednisolone, 2-3 weeks
108
define trigeminal neuralgia
Severe, unilateral “electric” pain along distribution of trigeminal nerve lines. Extremely increased risk in demyelinating disease. Attacks last seconds.
109
Pathophysiology of trigeminal neuralgia
Vascular loop (MC superior cerebellar artery) compresses nerve near nerve root entry zone. Compression causes poor conduction along nerve root, causing pain.
110
common triggers of trigeminal neuralgia pain
Light touch (washing, shaving, brushing teeth) - Talking - Cold weather - Spicy food - Caffeine and citrus
111
What are the branches of the trigeminal nerve
Ophthalmic Maxillary Mandibular
112
Signs/Symptoms of trigeminal neuralgia?
Facial pain - Electric/stabbing pain - Very severe - Trigeminal distribution - Unilateral - Provoked (touch, cold etc)
113
Ix and Mx of trigeminal neuralgia
Clinical but can MRI brain (space occupying lesion, demyelination etc) Carbamazepine first line Surgery (microvascular decompression)
114
define cauda equina
Compression of the bundle of nerves below the end of the spinal cord (known as cauda equina). Causes bilateral lower limb weakness/saddle anaesthesia Medical emergency that requires immediate decompression
115
Signs/Symptoms of cauda equina
Severe lower back pain, bilateral lower limb weakness and reduced sensation. LMN signs! Saddle anaesthesia (numbness/reduced tone in perianal region, groin, inner thigh) Decreased reflexes and leg weakness/paralysis Erectile dysfunction Bladder/bowel dysfunction.
116
Ix and tx of cauda equina
URGENT MRI spine GOLD Emergency decompressive laminectomy (vertebra removal) within 24-48 hours, or permanent weakness/dysfunction
117
brief overview of anatomy of spine
Originates at base of medulla oblongata, exiting through foramen magnum, ending at conus medullaris at L2 Consists of 5 sections of vertebrae, with 31 spinal nerves arising from this - Cervical (7) - Thoracic (12) - Lumbar (5) (Spinal cord ends at L1, conus medullaris begins at L2) - Sacrum (5 - fused) - Coccyx (4 - fused) Beyond L2 are bundle of nerves called “cauda equina”
118
causes of spinal cord compression
Vertebral body neoplasms (thoracic most likely) - disc herniation - disc prolapse - infection - Trauma - Spinal stenosis
119
how do spinal cord lesions secondary and motor symptoms present?
Motor - Contralaterally Sensory - Ipsilaterally (same side)
120
what nerve roots are implicated in knee jerk, big toe jerk and ankle jerk reflexes?
Knee jerk - L3/4 Big toe - L5 Ankle - S1
121
signs/symptoms of spinal cord compression
Progressive (Hours-weeks/months) back pain and progressive leg weakness. Motor signs contralateral UMN signs above level of lesion LMN below level of lesion Sensory loss 1-2 cord segments below lesion level bladder/sphincter involvement is a late, bad signs
122
what levels are lesions in l5 nerve root compression and sciatica?
L5 nerve root compression - L4/L5 Sciatica - L5/S1
123
specific causes of peripheral neuropathy
DAVID Diabetes Alcoholism Vitamin B12 deficiency Infective/inherited (GBS/Charcot-Marie-Tooth) Drugs e.g. isonazid
124
what is brown sequard syndrome?
Damage to one half of the spinal cord, resulting in a specific pattern of symptoms: - Ipsilateral motor weakness Ipsilateral loss of proprioception (position sense), light touch, vibration at level of lesion Contralateral loss of pain and temperature sense below level of lesion
125
gold ix and mx of brown sequard
Investigations - EMG (electromyography) - MRI Spinal cord Management - Treatment of underlying condition - High dose steroids
126
Define/ explain pathophysiology of Charcot Marie Tooth syndrome
Group of inherited diseases (autosomal dominant) that cause axonal/myelin dysfunction. CMT1 and CMT2 most common CMT 1 - loss of myelin sheath (onion bulb myelin due to schwann cell repair) CMT 2 - Neuronal mitochondrial dysfunction = neurone death Causes atrophy of muscle when motor neurones affected
127
Signs/symptoms of charcot marie tooth
Weakness in lower legs and hands. Loss of muscle tone and reflexes Foot drop and claw hand Tingling/burning in hands and feet Thickened palpable nerves and hammer toes “Inverted champagne bottle” legs due to distal muscle wasting
128
Define Duchenne Muscular Dystrophy
X linked recessive condition characterised by severe muscle dystrophy due to absence of Dystrophin protein
129
Signs/symptoms of duchenne muscular dystrophy
Usually presents 3-5 years. - Weakness in pelvic muscles - Waddling gait - Gowers sign: due to inability to get up normally, they get into downward dog position then climb their hands up their legs to stand. - Fat calves due to buildup of fat and fibrotic tissue rather than muscle
130
Nerves implicated in wrist drop and claw hand
WD - Radial Cl - Ulnar (4th and 5th fingers claw)
131
What is Bells palsy
Acute, unilateral, idiopathic facial nerve paralysis. Aetiology unknown, but suspected HSV
132
How does Bells palsy present
LMN Facial nerve palsy -> Forehead affected (UMN spares upper face) - Post auricular pain - Altered taste - Dry eyes - Hyperacusis
133
How is Bell’s palsy treated
Prednisolone within 72 hours, maybe add antiviral most people with Bell’s palsy make a full recovery within 3-4 months
134
What is temporal arteritis
AKA Giant cell arteritis. Branches of carotid artery ( Occurs in >50, usually ~70. Strong association with Polymyalgia Rheumatica. Early recognition and treatment can minimise risk of complications e.g. permanent sight loss.
135
How does temporal arteritis present
Rapid <1 month onset Unilateral headache around temple/forehead Diminished/absent temporal artery Jaw claudication Blurred/double vision Optic disc pallor Scalp tenderness (Painful to comb) Fever, muscle aches, weight loss, loss of appetite
136
GCA typical presentation
50+ white female with unilateral temple headache, scalp tenderness (painful to comb), jaw claudication and vision changes.
137
Pathophys of GCA
Granulomatous vasculitis of large/medium arteries. Arteries become inflamed, intima is thickened and vascular lumen is narrowed. Usually cerebral (temporal) arteries affected: - Superficial temporal artery: Headache/scalp tenderness - Mandibular artery: jaw claudication - Ophthalmic artery: visual loss (retinal ischaemia)
138
Diagnostic criteria in GCA
3 of: - Over 50 - New headache - Temporal artery tenderness/diminished pulse - ESR Raised - Abnormal temporal artery biopsy
139
Management of GCA
High dose prednisolone Sight loss (amaurosis fugax!) Should be dealt with ASAP or could lead to permanent blindness Ischaemic cranial complications (Visual loss/stroke) Aortic aneurysm
140
In cases where long term steroids are given, what 2 systems should be protected and how is this done? GCA
GI (stomach and oesophagus) and Bones - PPI (omeprazole) - Alendronate (bisphosphonate) - Ca2+ and vitamin D
141
Define Polymyalgia Rheumatica symptoms ix mx
Condition that causes pain stiffness and inflammation in neck, shoulders and hips. Limits range of motion. Occurs alongside GCA often. Morning pain/stiffness in shoulders etc. Leads to fatigue, fever, weight loss, anorexia and depression Raised ESR but CK and EMG normal Managed with prednisolone
142
What is Broca’s area, and what does an injury of it cause?
Located in the frontal lobe of person’s dominant side (left in right handed people) and influences motor production of speech. Causes expressive aphasia - Patients can understand speech but can’t produce it themselves
143
What is Wernickes area and what does injury of it cause
Located in parietal and temporal lobe of person’s dominant side (left in right handed people) , influences understanding of speech and using correct words to express thoughts Causes receptive aphasia - Patients can produce speech but don’t understand the meaning of spoken words
144
What are Wernickes and Brocas areas supplied by?
Middle Cerebral Artery
145
What is a watershed area?
Areas furthest from blood supply, most susceptible to infarction
146
Define ischaemic stroke
Reduced cerebral blood flow due to arterial occlusion or stenosis. Account for 85% of all strokes. Consists of rapidly developing signs of cerebral dysfunction, lasting more than 24 hours, with no apparent cause.
147
Causes of ischaemic stroke
Disruption of blood supply secondary to: - Thrombus formation/ embolus - Atherosclerosis - Shock - Vasculitis - Hypercoagulability (thrombophilia)
148
Risk factors for stroke (9)
Male Old (>55) Black or Asian History of Ischaemic stroke or TIA Atrial fibrillation Sickle cell disease Combined contraceptive pill Carotid artery stenosis Smoking, obesity, HTN, T2DM
149
Define hemiparesis
Weakness or paralysis on one side of the body
150
Manifestations of an Anterior Cerebral Artery ischaemic stroke
Contralateral hemiparesis and sensory loss, affecting lower limbs>upper limbs
151
Manifestations of middle cerebral artery stroke
Contralateral hemiparesis and sensory loss affecting upper limbs>lower limbs. Aphasia if affecting Broca or Wernickes areas in dominant hemisphere Homonymous hemianopia (visual field defect in same side of both eyes)
152
Manifestations of Posterior Cerebral Artery stroke
Contralateral homonymous hemianopia with macular sparing (preservation of central visual field) Contralateral loss of pain and temperature
153
Manifestations of Vertebrobasilar artery stroke
Cerebellar signs (intention tremor, nystagmus, hypotonia) Reduced consciousness Quadriplegia
154
Manifestations of Webers syndrome (midbrain infarct)
Oculomotor palsy and contralateral hemiplegia
155
Manifestations of Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)
Ipsilateral facial loss of pain and temperature Ipsilateral Horner’s syndrome: miosis, ptosis, anhidrosis Ipsilateral cerebellar signs Contralateral loss of pain and temperature
156
What is lacunar stroke?
Stroke affecting small branches of middle cerebral artery. Causes one of the following: Pure motor loss pure sensory loss, ataxic hemiparesis
157
What is pronator drift
Ask patient to raise arms. On the affected side, palm and arm will face inward and downwards. Suggests muscle weakness. (Symptoms contralateral to affected brain side)
158
What assessment system is used in acute strokes
ROSIER (Recognition of Stroke In Emergency Room) Uses symptoms as + points and mimics (syncope, seizure activity) as - points
159
Investigations on stroke presentation
Assessment using ROSIER scale (stroke possible if >0) Non contrast CT head (rule out haemorrhagic stroke) CT Angiogram (identify occlusion - hypoattenuation of brain parenchyma, loss of matter differentiation)
160
How do strokes appear on CT
Ischaemic - Darkness of brain parenchyma Haemorrhagic - Brightness surrounded by darkness (blood surrounded by oedema)
161
Management of ischaemic stroke
Once haemorrhagic ruled out: - IV Alteplase if presents within 4.5 hours - Mechanical thrombectomy if after 4.5 hours Then: 300mg Oral aspirin daily for 2 weeks then clopidogrel lifelong daily
162
What are the driving rules in ischaemic stroke
Patients must not drive car for 1 month after TIA or stroke, or 1 year for HGV
163
What classification system is used in stroke?
Bamford classification - categorises stroke based on area of circulation affected. Total anterior circulation stroke - Anterior/middle cerebral artery (all 3 - Unilateral weakness of face,arm or leg, homonymous hemianopia, higher cerebral dysfunction) Partial anterior circulation stroke - only part of anterior circulation (2 out of 3 symptoms) Lacunar - Either: All sensory, all motor or ataxic hemiparesis Posterior circulation syndrome (1 of cranial nerve palsy, bilateral motor/sensory defecit, eye movement disorder, homonymous hemianopia)
164
Scoring system for risk of stroke after Atrial Fibrillation
CHA2DS2 VASc
165
DEFINE TIA
Transient Ischaemic Attack. Acute neurological dysfunction that has a sudden onset and resolves in less than 24 hours. NOT a stroke as involves ischaemia not infarction
166
Symptoms of TIA
Contralateral numbness, face drooping, dysphasia, vision loss Amaurosis Fugax Same as stroke but lasts less than 24 hours and no lasting effects
167
What acronym helps identify stroke in public
FAST Face Arms Speech Time
168
Define amaurosis fugax with pathophysiology and causes
Short lived blindness in one eye described as “curtain coming down over vision”. Due to temporary reduction in internal carotid or central retinal artery leading to ischaemia of the retina. Occurs in GCA, Stroke, AF
169
What risk score should be completed after TIA
ABCD2 - risk of stroke after TIA Age >60 BP >140/90 Clinical features (unilateral weakness =2, just speech disturbance =1) Duration >60mins =2, 10-59mins =1 > 6 predicts stroke, immediate referral 4 requires referral
170
MX OF TIA
1st line - 300mg Aspirin daily for 2 weeks - Clopidogrel daily long term - Atorvastatin ABCD2 score to assess stroke risk
171
What is it called when 2 TIAs happen in close proximity
Crescendo TIAs. Requires urgent referral
172
What are the layers over the brain called
Meninges of the brain Dura mater Arachnoid Pia mater (innermost layer)
173
What are the types of haemorrhagic stroke
Extradural haemorrhage - bleeding above dura mater Sudural haemorrhage - bleeding between dura and arachnoid Subarachnoid haemorrhage - bleeding between arachnoid and pia mater Intracerebral haemorrhage - Bleeding within cerebrum
174
Risk factors for haemorrhagic stroke (6)
Head injury Hypertension Aneurysms Brain tumour Connective tissue disorder Family history
175
General symptoms of haemorrhagic stroke
Reduced GCS Headache Vomiting Seizures One sided arm/leg/face weakness/paralysis
176
Give the scoring system for unconsciousness
Glasgow Coma Scale - assessment of eye opening, verbal and motor response. Minimum score 1 per category
177
Give the scoring system for consciousness
Glasgow Coma Scale - assessment of eye opening, verbal and motor response. Eye out of 4 Verbal out of 5 Motor out of 6 Minimum score 1 per category
178
Glasgow coma scale scoring system in detail (not sure if need to know but probably helpful to have decent idea)
Eye opening 4 - Spontaneous 3 - To speech 2 - To pain 1 - None Verbal response 5 - Orientated 4 - Confused conversation 3 - Inappropriate words 2 - Incomprehensible sounds 1 - None Motor response 6 - Obeys command 5 - Localises to pain 4 - Withdraws to pain 3 - Abnormal flexion to pain 2 - Extension of upper and lower limbs to pain 1 - No response
179
why might someone get a brain abscess?
extension of sepsis from middle ear or sinuses trauma or surgery to scalp penetrating head injury embolic event from endocarditis
180
presenting sx of brain abscess
depend on site of abscess - if motor cortex will present earlier mass effect on brain and raised icp headache: dull persistent fever: poss absent. not swinging pyrexia though focal neurology: oculomotor nerve palsy or abducens nerve palsy secondary to raised icp nausea papilloedema seizures
181
how would you investigate for brain abscess
ct scanning
182
how would you manage for brain abscess
surgery - craniotomy - debride abscess cavity. abscess can reform because head is closed after abscess drainage iv abx: 3rd gen cephalosporin+ metronidazole icp manage: dexamethasone
183
features of encephalitis
fever headache psychiatric sx , seizures, vomiting focal features: aphasia altered cognition/conciousness. unusual behaviour. peripheral lesions: like cold sores no relationship to presence of HSV encephalitis
184
pathophysiology of encephalitis
hsv-1 - 95% adult cases affects temporal and inferior frontal lobes
185
ix encephalitis
csf - lymphocytosis, elevated protein pcr: HSV,VSV,ENTEROVIRUSES neuroimaging: CT - medial temporal and inferior frontal changes - eg petechial haemorrhages normal in 1/3 of patients MRI is better hiv test swabs - causative organism, throat and vesicle swab EEG: lateralised periodic discharges at 2Hz
186
mx encephalitis
intravenous aciclovir start in all suspected encephalitis cases - hsv and vsv ganciclovir - cmv
187
comps of encephalitis
lasting fatigue/prolonged recovery headache, chronic pain, learning disability, change to memory, personality, mood , cognition. movement disorder sensory disturbance siezure hormonal imbalance
188
ci of lp in encephalitis in kids
gcs below 9 haemodynamiccaly unstable active seizures post-ictal
189
causes of encephalitis in kids
non infective: autoimmune mc : viral bacterial and fungal - rare mc: hsv. hsv-1 from cold sores. in neonates: hsv-2 from genital herpes from birth. vzv: chicken pox,cmv associated with immunodeficiency. ebv: infectious monucleosis, adenovirus, influenza virus. polio, mumps, rubella, measles - all can cause it too.
190
hsv encephalitis - typically affects with lobes
temporal
191
what is shingles herpes zoster?
acute unilateral painful blistering rash caused by reactivation of varicella-zoster virus - vzv. (following vzv infection, chickenpox) virus lies dormant in dorsal root or cranial nerve ganglia.
192
risk factors of shingles
increasing age hiv: strong rf 15* more common other immunosuppressive conoditions: steroids, chemo
193
most common affected dermatomes in shingles
t1-l2
194
features of shingles
prodromal period: - burning pain over affected dermatome for 2-3 days. -pain might be severe and sleep - 20% pts experience fever, headache, lethargy rash - erythematous, macular rash over affected dermatome -quickly becomes vesicular - characteristically well demarcated by dermatome dont cross midline. " bleeding" in adjacent areas might be seen. clinical diagnosis
195
how would you manage shingles - herpes zoster
avoid pregnant women and immunosuppresed - contagious infectious until vesicles crusted over, 5-7 days after onset. covering lesions reduces risk. analgesia: - 1st line para and nsaids - if not : neuropathic agent like amitriptyline - oral corticosteroids - in 1st 2 weeks in immunocompetent adults with localised shingles if pain severe. antivirals - within 72 hrs for most patients, unless pt under 50 and mild truncal rash with mild pain - aciclovir , famciclovir, valaciclovir
196
benefit of prescribing antiviral in shingles - herpes zoster
reduced incidence of post-herpetic neuralgia
197
complications of shingles -herpes zoster
postherpetic neuralgia herpes zoster opthalmicus - ocular division of trigeminal nerve herpes zoster oticus - ear lesions and facial paralysis
198
malaria is caused by?
plasmodium protozoa spread by female anopheles mosquito: 4 diff : plasmodium falciparum - most. plasmodium vivax - 2nd - benign malaria plasmodium ovale plasmodium malariae
199
malaria protects from what diseases?
sickle-cell trait g6pd deficiency hla b53 absence of duffy antigens
200
falciparum malaria - mc - most severe type: features - classic triad why do they occur every 48 hrs?
paroxysms of fever chills and sweating. every 48 hrs because erythrocytic cycle of plasmodium falciparum parasite. fever high intermittent. - possible rigors too. non specific: malaise,headache,myalgia
201
general features of falciparum malaria
fever - cyclical - sweating and sometimes rigors. gi: -anorexia,n+v, abdo pain. diarhoea poss , mc in kids. poss mild jaundice and occasional pruritus resp: cough, poss mild tachypnoea msk: generalised body aches and joint pain neuro: headache. dizziness and sleep disturbance. cv: tachy, hypotension more typical of severe malaria. haem: thrombocytopenia most significant haematological finding. mild anaemia poss renal: aki associated with severe malaria. non severe : mild-moderate increase in creatinine or blood urea nitrogen levels
202
features of severe falciparum malaria how to treat
schizonts on blood film parasitaemia >2% hypogly acidosis temp over 39 severe anaemia iv artesunate if parasite count over 10% then exchange tranfusion shock might show bacterial septicaemia
203
comps of malaria falciparum
cerebral malaria: seizures, coma acute renal failure: blackwater fever, secondary to intravascular haemolysis ards hypogly dic
204
how would you manage falciparum malaria?
uncomplicated falciparum: 1st line: artemisinin-based combo therapy (acts) - artemether+ lumefantrine, artesunat+ amodiaquine, artesunate+ mefloquine, artesunate + sulfadoxine-pyrimethamine, dihydroartemisinin + piperaquine
205
mc non falciparum malaria
vivax - central america and indian subcontinent. then ovale (africa) and malariae. knowlesi - south east asia
206
features of non falciparum malaria
fever headache splenomegaly vivax/ovale: cyclical fever every 48 hrs. malariae: cyclical fever every 72 hours. associated with nephrotic syndrome. ovale and vivax: hypozoite stage : relapse after tx.
207
how would you treat non falciparum malaria?
artemisinin-based combo therapy (act) or chloroquine if chloroquine resistant. act avoid in pregnancy. ovale/vivax: primaquine after acute tx with chloroquine to destroy liver hypnozoites and prevent relapse
208
incubation period of malaria
1-4 weeks after exposure. vivax and ovale can lie dormant upto 4 yrs
209
how do you diagnose malaria
blood film. edta bottle. 3 negative samples over 3 consecutive days needed to exclude.
210
side effect of primaquine
can cause severe haemolysis in g6pd pts
211
doxycline - use in malaria when to give etc side effedcts
broad spect abx se: diarrhoea , thrush. skin sensitivity to sun take 2 days before until 4 weeks after endemic area travel.
212
antimalarial meds
proguanil with atovaquone doxycycline mefloquine - psych side effects. - anxiety,dep,abnormal dreams chloroquine with proguanil
213
general advice preventing malaria
mosquito spray 50% DEET spray nets and barriers antimalarial meds
214
metastatic brain cancer can spread from?
lung - MC breast bowel skin - namely melanoma kidney
215
features of brain tumour
poss asx progressive focal neurological symptoms raised icp
216
features of raised icp
headache contant worse at night or on waking or coughing/straining. vomiting papilloedema on fundoscopy (paton lines) altered mental state ptosis unilateral visual field defect 3rd and 6th nerve palsy
217
with papilloedema what do u see on fundoscopy?
blurring of optic disc margin engorged retinal veins haemorrhages around optic disc paton lines - creases in retina around optic disc loss of venous pulsation elevated optic disc
218
what is a glioma?
tumour of glial cells in brain/spinal cord. support/surround neurones. include: astrocytes,oligodendrocytes, ependymal cells. grade 1-4. 4 (glioblastoma multiforme)
219
3 types of glioma
astrocytoma - mc and aggressive is glioblastoma oligodendroglioma ependymoma
220
gliobastoma multiforme prognosis imaging histology tx
solid tumour with central necrosis and a rim that enhances contrast. pleomorphic tumour cells border necrotic areas surgery and postop chemo and/or radio. dex: oedema
221
what is a meningioma? histology ix tx
tumour of meninges. benign mass effect. = raised icp arise from arachnoid cap and typically located next to dura. spindle cells in concentric whirls and calcified psammoma bodies. CT: contrast enhancement MRI tx: RADIO/ SURGERY
222
tell me about pituitary tumours. press on what? sx? mx
benign optic chiasm press - bitemporal hemianopia cause hormone def or release excessive hormones lead to: - acromegaly -hyperprolactinaemia - cushings disease - thyroxicosis transphenoidal surgery radio bromocriptine - block excess prolactin somatostatin analogue - block excess GH
223
symptoms of cerebellar disease
D - dysdiadokinesia, dysmetria, “drunk” A - ataxia - limb,truncal N - nystagmus - horizantal = ipsilateral hemisphere I - intention tremor S - slurred staccato speech, scanning dysarthria H - hypotonia
224
unilateral cerebellar lesions cause what signs?
ipsilateral
225
causes of cerebellar disease
friedreichs ataxia neoplastic: cerebellar haemangioma stroke alcohol ms hypothyroid drugS: phenytoin, lead poisoning paraneoplastic: 2 to lung cancer
226
What is normal pressure hydrocephalus?
reversible cause of dementia in elderly. 2 to reduced csf absorption at arachnoid villi. could be due to head injury, subarachnoid haemorrhage or meningitis
227
classic triad of normal pressure hydrocephalus
urinary incontinence dementia and bradyphrenia gait abnormality sx develop over a few months
228
imaging for normal pressure hydrocephalus
hydrocephalus with ventriculomegaly in absence of ,or out of proportion to , sulcal enlargement
229
how would you manage normal pressure hydrocephalus comps of this tx
ventriculoperitoneal shunting seizures infection intracerebral haemorrhage
230
What is Cerebral Palsy?
non-progressive lesion motor pathways in developing brain. disorder of movement and posture.
231
causes of cerebral palsy antenatal intrapartum postnatal
antenatal 80% - cerebral malformation -congenital infection (rubella, toxoplasmosis, CMV) intrapartum 10% = - birth asphyxia/trauma -preterm birth postnatal 10% - intraventricular haemorrhage -meningitis -head trauma
232
classifying cerebral palsy 4 different types
spastic 80% - hemiplegia, diplegia or quadriplegia -increased tone (hypertonia) and reduced function resulting from damage to UMN dyskinetic: - damage to basal ganglia and substantia nigra -athetoid movements and oro-motor problems . muscle tone problems (hypertonia/hypotonia) causing the athetoid etc. ataxic: - caused by damage to the cerebellum with typical cerebellar signs - problems with coordinated movement due to above. mixed: mixed of spastic,dyskinetic and/or ataxic features.
233
patterns of spastic cerebral palsy
monoplegia: 1 limb affected hemiplegia: one side of body affected diplegia: 4 limbs affected by mostly legs quadriplegia: neck down all 4 limbs - with seizures, speech disturbance and other impairements
234
what non-motor problems might a cerebral palsy patient have?
learning difficulties - 60% epilepsy 30 squints 30% hearing impairement 20
235
How would you manage cerebral palsy?
tx spasticity: -oral diazepam -oral and intrathecal baclofen (muscle relaxant), botulinum toxin type A , orthopaedic surgery and selective dorsal rhizotomy. anticonvulsants, analgesia prn physio - stretch and strength muscles prevent muscle contractures. OT SLT DIETICIAN - peg feeding poss? ORTHO SURGEON - release contractures or length tendons (tenotomy) glycopyrronium bromide: excessive drooling. anti-epileptic - seizures
236
what condition makes children at risk of developing cerebral palsy?
hypoxic-ischaemic encephalopathy
237
signs and symptoms of cerebral palsy
failure to meet milestones learning difficulty feeding or swallowing problems problems with coordination, speech or walking increased/decreased tone, generally or in specific limbs hand preference below 18 months .
238
based on neuro exam what to each of these indicate: hemi/di plegic gait broad based gait/ataxic gait high stepping gait waddling gait antalgic gait
UMN lesion cerebellar lesion foot drop/lmn lesion pelvic muscle weakness due to myopathy indicates localised pain
239
with a UMN lesion tell me about: inspection tone power reflexes
muscle bulk preserved hypertonia slightly reduced brisk
240
with a lmn tell me about: inspection tone power reflex
reduced muscle bulk with fasciculations hypotonia dramatically reduced reduced
241
complications and associated conditions of cerebral palsy
learning disability epilepsy kyphoscoliosis muscle contractures hearing and visual impairment gastro-oesophageal reflux
242
what is hypoxic ischaemic encephalopathy?
neonates. hypoxia during birth.
243
causes of HIE
anything that leads to asphyxia (deprivation of oxygen) to the brain. eg: maternal shock -intrapartum haemorrhage -prolapsed cord - causing compression of the cord during birth nuchal cord - where the cord is wrapped around the neck of the baby
244
grading HIE mild moderate severe
sarnat Staging mild: - poor feeding, generally irritability and hyper-alert -resolves within 24 hours -normal prognosis moderate: - poor feeding, lethargic, hypotonic, seizures -can take weeks to resolve -up to 40% develop cerebral palsy severe: - reduced gcs, apnoeas, flaccid and redcued or absent reflexes -upto 50% mortality -upto 90% develop cerebral palsy
245
when to suspect HIE
neonate acidosis (ph under 7) on umbilical abg poor Apgar score features of mild,mod,severe HIE evidence of multi organ failure.
246
how would you manage HIE
supportive care with neonatal resus optimal ventilation, circulatory support, nutrition, acid base balance and seizure tx. therapeutic hypothermia - protect brain from hypoxic injury.
247
what is horners syndrome?
combo of sx that happen when group of nerves known as sympathetic trunk is damaged. eye and surrounding area on 1 side of face.
248
features of horners syndrome
miosis - small pupil ptosis enophthalmos - sunken eye anhidrosis - loss of sweating one side
249
using anhidrosis to decipher where the lesion is for horners syndrome
face arm and trunk: central lesion face: pre-ganglionic no anhidrosis: post-ganglionic
250
central lesion causes of horners pre ganglionic post ganglionic
stroke, syringomyelia, ms, tumour, encephalitis pancoasts tumour , thryoidectomy, trauma, cervical rib carotid artery dissection, carotid anerusym, cavernous sinus thrombosis, cluster headache
251
heterochronic - difference in iris colour is seen in what?
congenital horners
252
horners - what are apraclonidine drops
alpha adrenergic agonist cause pupillary dilation produces mild pupillary construction in normal pupil.
253
What is epilepsy? types
seizure tendency. transient episodes of abnormal electrical activity in brain. generalised tonic-clonic focal seizures absence atonic myoclonic infantile spasms febrile convulsions
254
What are febrile convulsions? age of onset mc type of seizure here clinical features
seizures provoked by fever in otherwise normal kids. 6 months and 5 years. tonic-clonic usually occur early in viral infection as temp rises rapidly seizures brief: last less than 5 mins
255
types of febrile convulsion simple complex febrile status epilepticus
simple: - less than 15 mins -generalised seizure -typically no recurrence within 24 hours -should be complete recovery within an hr complex: - 15-30 mins -focal seizure -may have repeat seizures within 24 hours febrile status epilepticus : - over 30 mins
256
Mx of Febrile Convulsion following a seizure ongoing
admit if first or features of complex seizure phone ambulance if seizure over 5 mins. benzodiazepine rescue med: rectal diazepam or bvuccal midazolam regular antipyretics: dont reduce chance of them occuring
257
prognosis of febrile convulsions
risk of another one is 1 in 3. depends on: age of onset under 18months fever under 39 shorter duration of fever before seizure fhx of them
258
rf for developing epilepsy post febrile convulsions
fhx of epilepsy complex febrile seizures. background of neurodevelopmental disorder if no rf@ 2.5% risk of developing it. if kids have all 3 features 50% risk
259
what is benign rolandic epilepsy? how to ix and what does it show prognosis features
form of childhood epilepsy occurs between 4 and 12. EEG - centrotemporal spikes excellent prognosis - seizures stop by adolescence seizures at night. partial seizures (paresthesia affect face) but secondary generalisation may occur (parents may only report tonic-clonic movements)
260
Using Contraception in epilepsy what factors are to be considered?
effect of contraceptive on effectiveness of anti-epileptic effect of anti-epileptic on effectiveness of contraceptive potential teratogenic effects of anti-epileptic if women becomes pregnant
261
if women is taking phenytoin carbamazepine barbiturates primidone topiramate oxcarbazepine what to do? for contraception in epileptic pt
ukmec 3 : the COCP and POP ukmec 2 : implant ukmec 1 : depo-provera, IUD,IUS use condom if COCP : min of 30 ug of ethinylestradiol
262
for lamotrigine if women takes what to do? contraceptionin epileptic pt
use condom ukmec 3 : cocp ukmec 1: pop, implant, depo-provera, Iud, ius if COCP: min or 30 ug of ethinylestradiol
263
what conditions are associated with epilepsy?
cerebral palsy: 30% have it tuberous sclerosis mitochondrial diseases
264
what is an alcohol withdrawal seizure? mechanism tx
pt hx of alcohol excess suddenly stopped drinking. 36 hours after drink cessation. give benzodiazepine after stopping. chronic alcohol enhances gaba mediated inhibition in cns and inhibits nmda-type glutamate receptors. alcohol withdrawal dose the opposite
265
what are psychogenic non-epileptic seizures?
pseudoseizures epileptic-like seizures but no electrical discharges. hx of mental health or personality disorder
266
define a focal seizure
partial seizure.- start in temporal lobe. start in a specific area , one 1 side of brain. varied awareness. 30 yr old women told by her husband she wakes at night, grunting sound, lip smacking, non responsive during ep. after minute falls asleep again. focal impaired awareness - explained above. classified into motor: jacksonian march non-motor : deja vu, jamais vu or other features like aura sx: affect hearing speech memory and emotions. hallucinations -memory flashbacks -deja vu doing strange things on autopilot
267
generalised seizure define
involve networks on both sides of the brain at onset. lose conciousness immediately. motor: tonic clonic non motor: absence specific types: -tonic clonic - grand mal - tonic -clonic -typical absence - petit mal - myoclonic: brief,rapid muscle jerks - atonic
268
unknown onset seizure - what is it?
unknown origin of seizure
269
focal to bilateral seizure - what is it
starts on 1 side of brain in specific area before spreading to both lobes previously called secondary generalised seizure
270
tell me about typical absence seizures: petit mal onset duration eeg tx prognosis
onset: 4-8 years duration : few-30 seconds. no warning, quick recovery: often many per day eeg: 3Hz, generalised, symmetrical sodium valproate, ethosuximide good prognosis: 90-95% become seizure free in adolescence
271
if a focal seizure happens starts in occipital lobe (visual) what happens?
floaters/flashes
272
if a focal seizure happens in parietal lobe what happens ? (sensory)
paresthesia
273
if a focal seizure happens in frontal lobe? (motor)
head/leg movements, posturing post-ictal weakness (todd’s paresis), jacksonian march (clonic movements travelling proximally)
274
if a focal seizure starts in temporal lobe what can i expect?
last around 1 min - automatisms (lip smacking/grabbing/plucking) common with/without impairement of conciousness or awareness aura in most: - rising epigastric sensation -psychic or experiental phenomena like deja vu , jamais vu -less common: hallucination (auditory,gustatory,olfactory)
275
sodium valproate is associated with what issue for maternal kids?
neural tube defects risk of neurodevelopmental delay in kids after maternal use of it. DONT USE IN PREGNANCY AND WOMEN OF CHILDBEARING AGE UNLESS NECESSARY.
276
which of the epileptic drugs is seen as least teratogenic or older antiepileptics?
carbamazepine
277
phenytoin is associated with what issue? antiepileptic what to give with it. this is to prevent what?
cleft palate vit k last month of pregnancy prevent clotting disorders in newborn
278
is breast feeding safe for mothers taking anti-epileptics? is there an exception to the rule?
yes NO BARBITURATES
279
women want to get pregnant epileptic what should they take and why?
folic acid 5mg per day well before pregnancy minimise risk of neural tube defects
280
briefly explain what an absence seizure is? tx
in kids. pt becomes blank stares into space and abruptly returns to normal. unaware of surroundings, wont respond. 10-20 seconds. stop when they get older 1st line: ethosuximide 2nd line: m - sodium valproate f: lamotrigine or levetiracetam carbamazepine - exacerbate absence seizures
281
how would you tx focal seizures ?
1st line : lamotrigine or levetiracetam 2nd line: carbamazepine, oxcarbazepine or zonisamide
282
the rules are you start antiepileptics after second seizure. in what case would you start after first?
pt has neuro deficit brain imaging shows structural abnormality EEG shows unequivocal epileptic activity. pt or their fam or carer consider the risk of having a further seizure unacceptable
283
generalised tonic clonic seizure tx?
male: sodium valproate female: lamotrigine or levetiracetam under 10, unlikely to need tx when old enough to have kids or women unable to have children can be given sodium valproate first line.
284
how to atonic seizures present? tx?
drop attacks. brief lapse in muscle tone. no more than 3 minutes. childhood begin. indicative of lennox-gastaut syndrome. mx: - m: sodium valproate - f: lamotrigine
285
how do myoclonic seizures present? tx?
sudden brief muscle contractions - sudden jump. awake during. happen in kids as part of juvenile myoclonic epilepsy. tx: - m - sodium valproate - f : levetiracetam
286
rescue medication for epilepsy if they dont terminate spontaneously ie after 5-10 mins
benzodiazepines like diazepam administer rectally or intranasally/under tongue. if still fits: status epilepticus. - medical emergency - hospital tx required. mx: further benzodiazepine med, infusion of antiepileptic or general anesthetic.
287
ix for epilepsy
good history eeg: typical patterns of it. after the second simple tonic clonic do. MRI brain: structure of brain. ecg - exclude heart problems blood electrolytes - sodium, potassium, calcium , magnesium bg: hypoglycaemia and diabetes blood cultures, urine cultures and lp where sepsis, encephalitis or meningitis is suspected
288
general advice for epileptic patients
take showers not baths cautious with heights, traffic, heavy/hot/electric equipment be very catious with swimming unless seizures well controlled and they are closely supervised.
289
mx of seizures physically
pt in safe position - carpeted floor recovery position if poss something soft under head remove obstacles that could lead to injury note the time at start and end call ambulance if more than 5 mins or 1st seizure.
290
what is status epilepticus? mx: medical options in community ?
med emergency seizure lasting more than 5 mins or 2 or more seizures without regaining consciousness in interim. ABCDE approach secure airway high conc ox assess cardiac and resp function check bg levels iv access - insert cannula iv lorazepam - repeated after 10 mins if the seizure continues. if persist final step is iv phenobarbital or phenytoin. intubation and ventilation to secure airway- transfer to icu. med options in community: - buccal midazolam - rectal diazepam