Neurology Flashcards
Mixture of fluent and expressive aphasia
Arcuate fasciculus lesion
Gene mutations PD
GBA (glucocerebrosidase)
Dopamine agonists
Impulse control disorders
Nausea
Ortho static hypotension
Confusion and hallucinations
memantine
amantadine
NMDA glutamate receptor antagonist
Increase dopamine release
Rx: Alzheimer’s
livedo reticularis
Insomnia
leg oedema
blurred vision
Hot cross bun sign
MSA
Humingbird sign
PSP
MSA
Alpha synucleiopathy
Erectile dysfunction
Urinary incontinence
Postural hypotension
Progressive supranuclear palsy
Early falls
supranuear down gaze palsy
Postural instability
Tau protein
Corticobasal syndrome (Parkinson’s plus)
Apraxia
Frontal lobe dementia
SN gaze palsy
Alien limb
Natalizab
Alpha 4 interim antagonist MS RX Selective adhesion molecule inhibitor Decrease in relapse rate PML risk
Almtuzumab
Mab to CD52 (B cells)
MS Rx
Decreased relapse
No PML
ITP
Autoimmune disease
Ocrelizumab
MS treatment
Anti CD20 mAb
Depletes B calls
Fingolimob
MS Rx
Down regulates sphingosine-1-phosphate receptor
Decrease relapse rate
Heart block
PML
Macular oedema
Optic neuritis
Pain on eye movements Decreased acuity Impaired colour vision RAPD Scotoma
Gerstman syndrome
Brodman 39 and 40 near temporal and parietal junction
Left angular and supramarginal gyrus
Dysgraphia
Dyscalcula
Finger agnosia
Basilar syndrome
EOM abnormalities
Dilated pupil
GCS
Staggered course
Anterior spinal artery infarct
Loss of power distally
Loss of temp/pain
Posterior cord unaffected
Causes of lobar haemorrhage
Cerebral amyloid angiopathy
HLA subtype Carbamazepine
HLA B1502 SJS syndrome
HSV encephalitis location
Bilateral temporal
Lambert Eaton syndrome association
50% paraneoplastic
Mainly SCLC
IgG Abs against Ca channels
In Parkinson’s disease excessive amounts of which protein accumulates in the central nervous system
Alpha synuclein
In Alzheimer’s disease excessive amounts of which protein accumulates in the central nervous system?
Tau protein is seen in Alzheimer’s and forms the typical Neurofibrillary tangles
Amyloid
mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS)
Stroke like symptoms
Seizures
Migraine
Alpha synucleiopathies
MSA
Lewy body Dementia
Parkinsons Disease
Gerstmann’s syndrome (dominant parietal)
- Agraphia
- Acalculia
- FInger agnosia
- Left-right confusion
Non-dominant complete MCA lesion
- Inattention (visual, sensory, motor)
- Anosognosia
- Prosopagnosia
- Emotional speech
- Motor impersistence/apraxia
Prosopagnosia
Inability to recognise faces
Anosognosia
Denial of neurological defect
Superior division MCA
- Brocas aphasia if dominant side
- Contralateral Weakness face and arm > leg
- Contralateral Sensory loss face> arm
- Hemi-neglect if non noninant
Inferior division of MCA infarct
- Contralateral homonomous hemianopia
- Non-dom: Apraxia
- Dom: Wernicke’s area
ACA infarct
- Ciontralateral aralysis of leg>arm
- Cortical sensory loss of lower limb
- Contralateral primitive reflexes (FL)
- Abulia (FL)
- Urinary incontinence (FL)
Left PCA infarct
- Homonomous hemianopia
2. Alexia without agraphia
Right PCA infarct
- Homonomous hemianopia
- Prosopagnosia
- Visual neglect
Blood supply to lacunar areas
MCA penetrating arteries
Anton’s syndrome
Cortical blindness
Alexia
Unable to recognise individual words
Kimmelstiel Wilson nodules
Diabetic nephropathy
Wire loop lesions
Lupus nephritis
Loss of pain and temperature on left and right (face and body opposites)
Lateral medullary syndrome of Wallenberg
PICA/vertebral artery occlusion
Beta transferritin in rhinnorea fluid
CSF leak
acute weakness with low potassium
periodic paralysis
In setting of calcim channel defect
Drug for MND and action
Riluzole
sodium channel blocker that inhibits glutamate release.
May slow progression of MND marginally
Phenytoin SEs
Osteoporosis ataxia nystagmus gingival hyperplasia coursening of facial features hormone dysfucntion bone marrow hypoplasia.
Vigabatrin
Drowsiness(most common)
neuropsychiatric symptoms
weight gain
visual field changes.
Miller fischer symptoms and treatment
Opthalmoplegia
Ataxia
Muscle weakness eith areflexia
No IVIG / treatment
Tauopathies
Progressive supranuclear palsy
Corticobasal dgeneration
Frontotemporal dementia
Alzheimer’s dementia (also amyloid)
Alpha-synucleinopathies
Lewy body
Parkinsons disease
Multi systems atrophy
Pathophysiology of tau
Abnormal phosphorylation of tau interferes with microtubule function, impairs axonal transport, and leads to tau aggregation into neurofibrillary tangles.
Where is CSF produced (mostly)
Choroid plexus
Anterior cord syndrome
Flexion injury or vascular injury (anterior spinal artery)
Proprioception and vibration spared
loss or motor and pan and temp below level of lesion
Central cord lesion
M - Motor>sensory
U - Upper extremity > lower extremity
D - Distal > proximal
E - Extension injury
Brown-sequard injury
Ipsilateral loss of motor and proprioception/vibration
Contralateral loss pain/temp
Sensory level nipples
T4
Sensory level umbilicus
T10
Nerve roots in the cauda equina
L1–L5 and S1–S5
Nerve roots in sciatic nerve
L4, L5, S1, S2, and S3
Treatment of benign intracranial hypertension
Weight loss
carbonic anhydrase inhibitor (acetazolamide )