Acute neurological disorders (ICP/Seizures) Flashcards
Intracranial regulation (ICR)
Effected by
- Impaired blood flow
- Damage to brain tissue
- Comprimised neurotransmitted (eg. parkinsons)
- Impaired glucose regulation
Monro-Kellie doctrine
Skull is rigid, therefore in high ICP, it will decrease CSF to compensate for blood/brain tissue
Cerebral perfusion pressure
CPP = MAP-ICP
= Pressure needed for adequate brain perfusion
Normal CPP = 70-90 mmHg
Effected by
i) Systemi BP
ii) ICP = high icp causes less perfusion
- caused by intracranial bleeding, cerebral edema, tumor
Normal ICP is 5-15, higher than 20 is concerning
Autoregulation will fail if CPP is too low
Compensatory mechanism
1) CSF volume = Monro-Kellie doctrine, where less CSF produced and it enters spinal subarachnoid space to make space
2) Autoregulation (cerebral vasodilation/vasoconstriction
= Fails when BP is outside 60-150 mmHg
Hypotension - severe ischemia
HTN - stroke/rupture
Increased ICP causes
1) Brain tissue - tumor, edema
2) Blood - hemorrhage/hematoma
3) CSF - Hydrocephalus, meningitis
Cerebral edema
Increased fluid in intracellular/extraccular spaces
Neurological cause - ischemia, hemorrhage, hypoxia, trauma, infection, hydrocephalus
Non-neurological cause - HTN, liver damage, HE
1) Vasogenic
BBB becomes dysfunctional as permeability increases, so things leak into the brain
Allows leakage of plasma protein, which draws water
Caused by brain tumors, trauma, abscesses, toxins
Clinical manifestation - focal neurological deficits, change in LOC, severe ICP increase
2) Cytotoxic/metabolic
Sodium/potassium pump fails and causes retention of sodium = Swelling and loss of function
Cyto= cell
3) Interstitial
In hydrocephalus when there is obstruction preventing outflow of CSF, so it moves to extracellular spaces instead
Increased ICP consequences
1) Cerebral edema
2) Compression of blood vessels, tissues, ventricles = ischemia
3) Tissue hypoxia = cell death
4) Acidosis from alctic acid
5) Brainstem compression
6) Brain herniation (fatal)
Clinical manifestations of increased ICP
1) Change in LOC
- Early sign
- Decrease in blood flow
2) Ocular signs
- Compression of oculomotor nerve 3
- Sluggish/no constriction
- Ptosis = dropping of eyelids
3) Change in VS
- Cushings triad
- Change in temp (hypothalamus)
4) Decrease in motor function
- Contralateral hemiparesis/hemiplegia
- Decorticate posturing = when herniating or about to, adducted arms, damage to hemisphere, thalamus and mid-brain
- Decerebrate posturing = Adducted arms, damage to upper brainstem
5) HA
- Compression of vessels or nerves
6) Vomiting
- Direct pressure on vomiting center in medulla
7) Seizures
Cushings triad
1) HTN - increased systolic, but ICP compresses blood vessels to the brain, which causes the SNS to activate and increase BP
- High CO/BP
2) Bradycardia
Baroreceptors releases BP is high, but CO is good, so tries to slow the HR (Stupid body)
3) Bradypnea
Cheyne-stokes = irregular HR with periods of apnea due to pressure on brainstem
Bacterial meningitis
Acute inflammation of the meninges (pia, arachnoid, dura)
- occurs iin children, older adults, high risk population
- More in winter (resp disease)
Enter through Upper respiratory tract or through wound in skull
Influenza flu decreases risk
Massive inflammatory response occurs = CEREBRAL EDEMA
as neutrophils enter the subarachnoid space and release cytokinetic inflammatory agents
CSF becomes thick and interferes with flow = HYDROCEPHALUS AND OBSTRUCTION
Clinical manifestation
- Fever, HA, N/V, seizure, cranial nerve dysfunction
- Nuchal rigidity (neck stiffness)
- Positive Kernig sign (pain when flexing knee)
- Photophobia
- Hemiplegia, hemiparesis, aphasia
Seizures
Electrical impulses
Epilepsy is chronic, seizure is abnormal
Risk factors include hypoglycemia, hypoxia, alcohol, electrolyte, barbiturate withdrawel, acidosis, dehydration, water intoxication
Other - brain injury where cord wraps around fetus, ifnection, metastiatic brain tumor
Generalized seizures
Effect both side of the brain, no warning signs occurs
