Neuro Review Flashcards
What is bacterial meningitis?
Inflammation of meninges secondary to bacterial infection
Causes of bacterial meningitis
Hemorrhagic spread, foreign body migration, extension of otitis media/interna (majority of cases), traumatic or iatrogenic inoculation
Diagnosis of bacterial meningitis
Clinical presentation, routine blood work, MRI (meningeal contrast enhancement), CSF (marked neutrophilic pleocytosis with intracellular bacteria, can be normal in chronic cases, only 33% bacterial growth), pyrexia only in 13% of cases
Prognosis of bacterial meningitis
Good prognosis (83% survival to discharge), with few/mild long-term neurological deficits.
Decerebrate
Extensor rigidity in all 4 limbs, patient comatose.
Severe midbrain lesion.
Poor to grave prognosis.
Decerebellate
Opisthotnus, flexed pelvic limbs.
Acute cerebellar lesion.
Better prognosis than decerebrate.
Menace
Afferent: ipsilateral CNII, contralateral thalamus and occipital cortex
Efferent: contralateral motor cortex, ipsilateral cerebellum, ipsilateral CN VII
PLR
Midbrain
Afferent: CN II
Efferent: CN III parasympathetic
Trigeminofacial reflex
Palpebral, vibraase, lip pinch
PONS
Afferent: CN V
Efferent: CN VII
Corneal reflex
PONS
Afferent: CN V (ophthalmic branch)
Efferent: CN VII (globe retraction, CN VII (Blink))
Physiologic nystagmus
PONS, midbrain
Afferent: CN VIII
Efferent: CN III, IV, VI
Gag reflex
Medulla
Afferent: CN IX, X
Efferent: CN IX, X, XII
Reactive Seizure
The normal brain’s natural response to a transient disturbance in function, usually metabolic or toxic in nature. Is usually reversable when the inciting cause is removed or corrected (i.e. hypoglycemia)
Epileptic Seizure
A manifestation of excessive synchronous epileptic activity of neurons in the brain.
Epilepsy
Recurrent seizures of at least two unprovoked epileptic seizures (of any type) in a 24-hour period, resulting from a disease in the brain causing a predisposition to generate epileptic seizures.
Cluster seizure
Two or more seizures within a 24-hour Period
Status Epilepticus
Continuous seizures or two or more discrete seizures between which there is incomplete recovery of consciousness, lasting at least 5 minutes. A neurologic emergency requiring immediate therapy
Focal seizure
Seizures that originate from a focus in one cerebral hemisphere and usually manifest localized or regional clinical signs, which may include involuntary or compulsive actions such as chewing, licking, and defensive or aggressive behavior.
How does status epilepticus cause neuronal necrosis?
In late SE, Cerebral blood flow decreased simultaneously as blood pressure decreases and cerebral metabolic rate (i.e. glucose and oxygen use) increases. This leads to ATP depletion and lactate accumulation.
Progressive intracranial diseases
- Inflammation (Granulomatous Meningoencephalitis)
- Nutritional Alterations (Thiamine Deficiency)
- Infection, Anomalous ( Hydrocephalus)
- Trauma
- Neoplasia
Normal intracranial pressure?
5-12 mmHg
Causes of increased ICP
TBI, Intracranial mass, inflammatory encephalopathy, status epilepticus, obstructive hydrocephalus, infectious/non-infectious causes
Cushing’s triad
-bradycardia
-hypertension
-irregular breathing
Chemical autoregulation of ICP
- PaCO2
- inc CO2 –> inc H+ ions –> stim cerebral vasodilation
- dec H+ –> vasoconstriction - PaO2
- dec PaO2 –> vasodilation –> inc CBF, CBV, ICP - CMRO2
- in high metabolic regions, pH alterations in perivasc space influence vasc tone
- inc H+ (lactic acidosis, other acids) –> inc CBF
Hypertonic saline
-reduces cerebral water content
-reduces blood viscosity -> improved cerebral perfusion
-beneficial effects on excitatory NTs as well on immune system
-Does not get reabsorbed in the kidneys so less likelihood of causing hypotension than mannitol
Mannitol
-Immediate plasma expanding effect, which reduced blood viscosity -> increases CBF
-Delayed osmotic effect occurs 15-30 min after administration, lasts 1-3 hours
-Free scavenging properties
Functions of CNS
- provide mechanical protection for brain by making it buoyant and reducing effective weight
- acid-base regulation
- intracerebral transport for AAs and sugars
- protects brain physically by buffering increases in ICP by translocating to extracranial space
Explain the pathophysiology of the Cushing’s reflex
-Intracranial hypertension leads to decreased cerebral blood flow, cerebral ischemia, and accumulation of CO2
-Decreased CBF and increased CO2 stimulates the release of catecholamines which causes systemic vasoconstriction and increased CO
-Baroreceptors sense hypertensive state -> vagally mediated bradycardia
