Hallmark signs of increased ICP [opposite of shock] - increased systolic BP - reduced pulse - reduced respiration

Neurology - Intro Flashcards by Fouche du Raan

Neural layers of the brain

Skull
Extradural space
Dura mater
Subdural space
Arachnoid
Pia mater
Blood/Brain barrier [sep CSF + Blood]

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Blood-Brain barrier

Endothelial cell of capillaries overlap
Protected by astrocytes
Allows only oxygen + nutrient exchange

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Neural damaging agents

Anoxia
Hypoglycaemia
Viral infection
Metabolic disturbance
Brain is susceptible to oxygen + glucose reduction - no storage tissue

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Neural Damage

2 Types:
Necrosis [assoc with acute function failure]
Atrophic [assoc with gradual function loss]

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Retrograde degeneration

Secondary neural damage

Main axon damage - degen of neuron as well as classical distal degen of axon

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Trans-synaptic degeneration

Secondary neural damage in closely integrated neuron systems

Neuron loss followed by degen of assoc neurons across synapses

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Satelitosis

Chromatolysis resutls increase in number of oligodendrocytes after damage of neurons

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Gliosis

Damage results in cells multiply + enlarging + increase in fibril production
Cells atrophy - leads to function reduction

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Consequence of nerve damage

Primary:
-destruction of myelin
-precedes axon damage
Secondary:
-loss of nerve cells + axon destruction

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Pathological mechanism of Cerebral Oedema

Initiating disorder = Cytotoxic components [cellular injury to neuron + glia]
Vasogenic components = capillary permeability leaks protein

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Raised Intracranial pressure

-expanding leasion [haeme + infarct]
-obstruction of CSF flow
Will lead to pupil dilation ipsilateral to mass/lesion

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Cushing’s Triad

Hallmark signs of increased ICP [opposite of shock]

increased systolic BP
reduced pulse
reduced respiration

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Stages of ICP increase due to expanding lesions

Compensation
Decompensation
Vasomotor paralysis
Secondary complications:
= Vascular damage [compres CRV - papilledema]
= Nerve pressure [N3 + N6][sudden oculomotor paralysis]
= CSF flow obstruction
= Skull bone changes if prolonged

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Cerebral Hypoxia

BP below 50 mmHg

Fast + permanent damage [Necrosis within 5min]

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Cerebral Infarction [stroke] pathogenesis

Precipitation condition - perfusion failure - infarction [ischaemic necrosis]

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Haematoma - def

accumulation of blood outside of vessel

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Subarachnoid haemorrhage

Caused by aneurysm at circle of Willis

If spreads leads to gen edema

Delayed complication of head injury

Haemorrhages from extradural haematoma
With time haematoma increases - increase ICP
Dura strips away from skull

Subdural Haematoma

results from rupture of bridging veins between arachnoid + dura [loosely connected]

Intracerebral Haematoma

Increase ICP - cerebral hypoxia

May lead to external leakage of CSF + Blood [ear + nose - potential entry for infection]

Hydrocephalus

Increase CSF + dilated ventricles
Mechanism:
- Overproduction of CSF
-CSF flow obstruction [can't reach subarachnoid space - ventricle swelling]
-Defective absorption of CSF

Intracranial Headaches

Only certain tissues are pain sensitive [stretching]

tumours causing stretching
assoc arterial dilatation [fevers, intoxication, hypertension]
meningeal inflamm + haemorrhage

Extracranial Headaches

All tissues are pain sensitive + nerve transference is common

Any Inflammatory disease
Prolonged muscle contraction
Vascular distention [migraine = episodic vasoconstriction with dilation]

Cluster Headache

Visual origin [squinting from uncompensated refractive error]
Dull ache= frontal + temporal
assoc with lacrimation

Tension Headache

assoc with eye strain | stabbing headache with prolonged muscle contraction [neck + shoulders]

Epilepsy

Grand mal = 1% [induced by flashing lights + stress] | Petit mal [10 min or less]

Cranial Nerves | On Occasion Our Trusty Truck Acts Funny, Very Good Vehicle Any How

``` Olfactory Optic Oculomotor Trochlear Trigeminal Abducens Facial Vestibulochochlear Glossopharynx Vagus Accessory Hypoglossal ```

Meningitis

Bacterial infection Stiff neck [excruciating pain] Fever Photophopia + headache

Encephalitis

Viral - Rabies, HSV, Polio, measles, VZV | Inner centre of brain affected

Variant Creutzfeld-Jacob [VCJ]

Prion = cause Degenerative neurological disorder Corneal transplant = possible mode of infection

Horner syndrome

Triad = Ptosis, Miosis,Anhidrosis | Disruption of ANS innervation of cervical ganglion at apex of lung

Multiple Sclerosis

Females 20 to 40 Affects Optic nerve + Cranials Neuro-transmission affected Diplopia + Optic neuritis + cortical blindness

Ataxia

Lack of muscle coordination | Affects speech,walking, swallow + eye movements

Tourettes - proprioception feature

Closing of eye leads to complete loss of balance

Myesthenia Gravis

Auto immune neuro muscular disorder Block ACh Ptosis with squint

Peripheral Neuropathy

Damage to peripheral nerves | Diabetes + Bells

Visual aura

possible feature of migraine | Distinguish from Scotoma [VF]

Cortical Blindness

total or partial loss of vision in normal looking eye Primary visual cortex damage Possible bilat post strokes

Visual agnosis

loss of ability to recognize objects Lesion to visual cortex Central achromatopsia Colour agnosia = no ID but can match

Alexia

Brain disorder = can read letters but not words | Distruction of left visual cortex, radiations + geniculate body

Foveal Hyperplasia

underdevelopment of the macula associated with albinism

charles bonnet syndrome [CBS]

common condition among people who have lost their sight | causes people who have lost a lot of vision to see things that aren't really there, known as visual hallucinations