Neurology

what percent of body weight is your brain

what percent of body weight is your brain

2%

what percent of your brain uses CO per min

15%

and 20% of all oxygen

what does your brain not do?

store oxygen

store nutrition (glycogen, Glucose)

recover nervous tissue injury (no centrioles)

Brain survival facts

w/o oxygen = 10 secs

apoptosis in 4-6 min

RAS

brain stem’s reticular activating system => wakefulness; activates higher centers of cerebral cortex

what will low RAS activity lead to?

lower awareness/ wakefulness; eg sleep

low RAS activity d/t pathology like decreased perfusion, altered metabolic state

=> altered consciousness (changed LOC). Decreased oxygenation = decreased fx of brainstem’s respiratory centers & decreased sensitivity to increased CO2 => irregular resps; apnea

brain injury caused by pathology (CVA, infection, tumor, trauma) sequelae:

ischemia, cerebral edema, metabolic acidosis, ICP

focal deficit

eg loss of hearing (eg: occipital tumor)

global deficit

eg: altered consciousness, stupor; coma; altered VS; declining autoregulation (eg: loss of protective reflexes- blink, urination, defecation

brain death criteria:

no motor response, no brainstem reflexes; apnea

(brainstem reflexes: gag, cough, doll’s eyes)

vegetative state:

does not meet brain death criteria

-damage to gray & white matter

• maintenance of brainstem reflexes; sleep-wake cycle; hypothalamic fx adequate to meet basic demands (temp reg)

• No awareness of self surroundings; inability to voluntarily interact; inability to reproduce behavioural responses

If some self awareness: ‘minimally conscious state’

hypoxia

deficient delivery of oxygen to the tissue

-often a result of hypoxemia (low blood oxygen) eg: anemia, toxicity…

• decreased oxygen delivery to ALL brain tissue

effects of hypoxia:

AGITATION, decreased LOC, seizures

Ischemia

lack of oxygen/ removal of waste within a TISSUE

focal or global

focal ischemia

CVA (deficit depends on the blood flow affected eg: speech affected

global ischemia simple

effects all brain tissue eg: metabolic acidosis (d/t severe asthma attack, ketoacidosis); or loss of CO (severe arrhythmia/MI)

Global ischemia (eg: no CO)

no nutrients & 02 delivery=> depletion of resources w/i 5 mins => brain injury

what compounding issues will be caused by Global ischemia

• cerebral edema

• electrolyte imbalances (Na, K, Ca)

  -electrolyte dysfx: excess intracellular calcium=> calcium cascade: protein breakdown, DNA injury, free radical formation, lipid peroxidation, mitochondrial injury= CELL DEATH

  -electrolyte dysfx => abnormal neurotransmitter secretion/ recycling=> accumulation of neurotransmitters or depletion of neurotransmitters

• ‘Watershed infarcts’- heightened focal damage to lowered flow regions (hippocampus)

• ‘Reperfusion injury - injury due to belated reperfusion, caused by inflammatory mediators/ toxic byproducts/ catecholamines/ nitric oxide

cranial cavity contents surrounded by the rigid skull :

brain tissue 80%

blood 10%

CSF 10%

monroe-kellie hypothesis

reduction of venous blood flow/ reduction in CSF content

trying to compensate to maintain homeostasis

normal ICP

0-15mmHg

CPP=

MAP-ICP

CPP= pressure gradient btw internal carotid artery & subarachnoid veins

-pressure required to perfuse the brain

-min CPP = 45mmHg (profound ischemia at <40 mmHg)

Increased ICP=>

obstructs fluid flow & displaces/injures brain cells

• S&S, life threatening: CUSHING’S TRIAD (HYPERTENSION, WIDE PP, BRADYCARDIA, IRR, RESPS)

• max impact=> ‘brain herniation’ (pressure displacement of brain tissue)

common caused of brain injury

CVA

Hematomas- epidural, subdural, intracerebral

Head injury, concussion

Infection

Brain tumor

=risk of cerebral edema=> increased ICP

(at first will be compensated by Monroe-kellie hypothesis)

two classes of cerebral edema

vasogenic and cytoxic

combination eg: complex head injury => hemorrhage + ischemia

Vasogenic cerebral edema

BBB compromise: Head injury, Hematoma; Hemorrhage; CNS infection=> inflammation => increased permeability = high ICP

cytotoxic cerebral edema

increased intracellular fluid shift: Hypoosmotic states/ electrolyte imbalance; ischemia leading to electrolyte imbalance=> increased H20 shift into cells= high ICP

what type of CVA accounts for 80% of CVA’s

Ischemic: thrombus/ embolus which is a clot

risk factors for Ischemic CVA

HTN, arterosclerosis, smoking, dyslipemia, stenosis, diabetes, atrial fib, drug side effects, age, genetics

what is TIA

angina of the brain- (a warning of CVA thrombus risk)

-transient episodes

-start CVA prevention

hemorrhagic stroke

bleed in the brain

Ischemic CVA tx if <3hrs since onset

thrombolytics

Ischemic CVA tx if <24hrs since onset

Thrombectomy (suck the clot out)

ass/ tx of ischemic cva as indicated

carotid endarterectomy or angioplasty

DRUGS: antiplatelets, anticoagulants

• tx hnt, dyslipemia

dysarthria

weak muscle control (slurred speach)

dysphagia

swallowing- problems w/ coughing or choking when eating or drinking

Aphasia

impairment of language, speaking

trouble saying the correct word (expressive aphasia)

trouble comprehending ( receptive aphasia)

Apraxia

moving the muscles needed in the correct order and sequence

Dyslexia

impairment of reading

Dysgraphia

impairment of writing

Agnosia

inability to recognize and identify objects or persons

Risk factors for Hemorrhagic CVA

htn, meds, age, arterial deficits (atriovenous malformation, aneurysm); bleeding disorders

1st S&S of hemorrhagic stroke

headache, vomiting, affected area S&S

-sudden onset

-sequelae: hemorrhage, ischemia, ICP, edema, necrosis, death

ER tx of CVA hemorrhagic

stabilize (intubate/02, sedate, eg. reverse anticoagulation); Osmotic diuretics/ hypertonic NS; optimize perfusion (htn tx), surgical evacuation

what type of solution would you give for hemorrhagic stroke

hypertonic NS: 3% NaCl IV solution

-osmotic diuretic: mannitol

AVM stands for

arteriovenous malformation

what is AVM

congenital defect in structural formation of cerebral vessels

-a bundle of arteries & veins lacking capillary network & lacking normal wall structure

=> high pressure arterial flow enters venous vessels rapidly (no capillaries) + the vessels are thinner than expected=> rupture (hemorrhage)

TX for AVM

radiation (gamma knife); embolization; surgical excision

if ruptured: tx per hemorrhagic CVA tx

Aneurysm

bulge in a vessel wall

Location:

• cerebral=> subarachnoid hemorrhage (80% in circle of Willis)

• Aortic Abdominal (AAA)

• Thoracic

Risk factors for an aneurysm

Atherosclerosis; htn; malformed vessels (congenitally thin intima or media); age

TX of unruptured Aneurysm

clipping, coiling, flow diversion

TX if cerebral aneurysm ruptures

hemorrhagic CVA

Aortic aneurysm

AAA

age is a factor: Elastin- not synthesized in elderly

TX if ruptures=> systemic bleed: fluids; surgery

GIVE NS or LR; infuse quickly

Hematomas

-Pool of blood

intracerebral: within cerebral lobes

causes: ruptured cerebral aneurysm, ruptured AVM, hemorrhagic CVA; head injury bleed

• ass/ w/ comorbidities: clotting dysfunctions (hemophilia, anticoagulants)

Epidural hematoma

btw dura and skull

-common cause: skull fracture injury

subdural hematoma

btw dura & subdural space

-most common: accel/decel injuries=> venous tearing

• Acute: sudden onset- high m&m d/t high ICP

• Subacute: slow onset-same danger

• Chronic: d/t brain atrophy = shrinking= tearing of veins= very slow onset

Sequalae of hematomas

Increased ICP, coma, necrosis

TX: decrease ICP; evacuate

Give mannitol to decrease ICP

Concussion is a

traumatic brain injury, induced by traumatic biomechanical forces

eg: direct impact; acceleration- deceleration forces

mild-moderate brain injury (inflammation rather than a bleed)

S&S of concussion

headache, amnesia, confusion, heightened sensitivities, nausea, irritability, insomnia, poor concentration/ memory

level of symptom is relevant to degree of injury

TX of concussion

low stimulation, slow return to normal ADLs, prevent second impact, if symptoms are severe tx focuses on relieving cerebral edema & high ICP

Post-concussion syndrome

-symptoms persist >3 months

more inflammation then bleed this is why you don’t see it on a CT scan

Infection

classified acc/ to anatomical structure infected & invading pathogen

-spread via blood OR direct entry (fracture, procedure/ surgery; other infected sites)

Structural, named by location:

• meninges= meningitis

• Brain parenchyma= encephalitis

• spinal cord= myelitiss

• brain & spinal cord= encephalomyelitis

Meningitis

Inflammation of: Pia matter, arachnoid, subarachnoid space (CSF space)

• Spread throughout due to infected CSF & it’s flow within CNS

2 Main types of meningitis

Bacterial (‘purulent’) & viral (lymphocytic)

common pathogens:

• Streptococcus pneumoniae (pneumococcus) - vaccine

• Haemophilus influenzae - vaccine

• Niseria meningitidis (meningococcus) - vaccine

• Listeria monocytogenes

• Group B streptococcus (etiology: newborns)

Mortality: step. pneumoniae highest @ 34%

-neurological deficits present @ 50%

sequalae of cerebral inflammation => CNS destruction

Meningitis pathology sequalae

severe inflammation=> BBB compromised=> inflammation causes further ‘capillary leaking’, cerebral edema, vascular congestion, cellular death; meningeal thickening=> meningeal adhesions= vascular congestion & decreased CSF outflow (hydrocephalus)

S&S of meningitis

fever, headache, stiff neck (nuchal rigidity), N&V, aches, CN deficits, seizures, Brudzinski sign (flexion of neck=> flexion of hip and knee); Petechial rash!

TX of meningitis

immediate broad spectrum abx & potent anti-inflammatories

• 3rd generation Cephalosporins; Penicillins; Vancomycin

• Glucocorticosteroids (Dexamethasone)

Where do you get a CSF sample

lumbar

what is a neoplasm

Brain tumor- abnormal cellular proliferation, which can metastasize

predominant demographic: 50-70yrs of age

primary brain tumor

originate in CNS- 2% of all cancer deaths

Metastatic brain tumor

originated in other tissues: lung or breast

upto 40% brain tumors have metastic origin

how are brain tumors graded

low grade & high grade

S&S of brain tumor

-focal disturbances

-global CNS effects if increased vol causes a CNS sequelae (cerebral edema, increases ICP, brain compression, blood & CSF floe disturbances)

General: headache, N&V, focal changes, LOC changes, seizures

DX and TX of tumor

MRI, EEG

TX: tumor origin, stage, size and location dependent

• surgery- excision of tumor

• radiation- gamma knife

• chemotherapy eg: alkylating agents (DNA damage)

what chemo med do you give for a brain tumor

Temozolomide (TMZ)

s/e: quickly replicating eukaryotic cells (hair loss, GI upset, bone marrow suppression, low blood cell counts)

How do you preserve brain fx

Tx the cause of the CNS event

eg: antibiotics; reperfusion w/ cerebral stenting; clot lysis (tPA); hematoma evacuation

TX the high ICP/ cerebral edema

• Hypertonic saline

• Osmotic diuretics

• Drainage of CSF (catheter into the 4th ventricle)

Maintain VS

seizure

spontaneous, abnormally synchronous electrical discharges from neurons in the cerebral cortex

Idiopathic seizure

genetic origin, no known acquired cause, aka epilepsy

eg: alteration in ion channel transport

TX: longterm anti-epileptic medications

Symptomatic seizures

due to a brain injury

=> results in altered action potential/neurotransmitter balance/ electrolyte balance

TX: short term anti-epileptic meds; tx underlying cause

3 main classes of seizures

Focal- specific group of neurons in one hemi

Generalized- both hemis involved eg: ebsence seizures, tonic-clonic seizures

Unknown- don’t fit either category

eg: febrile seizures

S&S of seizures

• loss of consciousness is very common

• aura – maybe experienced (aura itself is a focal seizure – aka ‘partial’ seizure)

• some present with ‘automatisms’ – repeating behavior (e.g. grimacing, lip smacking, patting,…)

• some are localized to one region of the brain, some span both hemispheres

• seizures may progress to other seizures (e.g. focal types to generalized types)

  • ‘evolving seizures’

• life threatening symptoms

  • Tonic convulsions cause constriction of muscles including the airway

  • Loss of consciousness impairs respiratory rate/depth

  • Large convulsions cause falls, flailing, … - prevent further injury!

  • Stimulation of ANS causes severe VS changes (e.g. tachycardia, hypertension, reflex hypotension, hyperventilation)

DX & TX of seizures

EEG, MRI

TX: benzodiazepines; barbituates; anticonvulsants

We want to increase GABA to calm the brain

Benzodiazepines

sedative-hypnotic’/ CNS depressant drug category (calming-sleep inducing) \n - Potentiate effects of GABA (inhibitory neurotransmitter) -chloride channel agonist

S/E: resp depression, drug-drug interactions, altered LOC & CNS activity, addictive

IV admin in ER/ continuous infusion

MEDS: -am/pam

• Clonazepam (Rivotril), Diazepam (Valium), Lorazepam (Ativan)

OD tx: receptor antagonist Flumazenil (Romazicon)

Status epilepticus

Any seizure type can progress to an unstoppable state which becomes life threatening = medical emergency

• Requires immediate treatment

• Tx 1st choice: benzodiazepines, IV

  • Diazepam, Lorazepam

Benzo abuse

• High drugs of recreational overuse/abuse

  • Not treating a clinical diagnosis

  • Used for ‘calming effects’ recreationally

  • E.g. Alprazolam (Xanax)

• ‘Roofies’

  • Flunitrazepam (Rohypnol)

  • Onset: 15 min

  • Duration: 4-6 hrs

  • Effect: confusion, sedation, amnesia

Barbituates

‘sedative-hypnotic’/CNS depressant drug category (calming-sleep inducing) \n potentiate effects of GABA (inhibitory neurotransmitter)

• chloride channel agonist

• highly addictive !

  • high degree of tolerance (e.g. induces own metabolism, down-regulation at receptors)

• s/e: respiratory depression, drug-drug interactions, altered LOC & CNS activity, risk of overdose (narrow TI)

• Meds: -barbital

  • Phenobarbital (Phenobarb), Pentobarbital, Secobarbital

  • OD tx: activated charcoal; sodium bicarbonate (urine alkalinization)

Anti-convuslants

Alter electrolyte mvt (Na or Ca)=> delay action potential, decrease neuronal activity

Decrease sodium cellular influx:

• Meds: Phenytoin (Dilantin); Carbamazepine (Tegretol), Valproic Acid (Valproate)

• s/e: arrhythmias; drug-drug interactions; bleeding (Vitamin K interference), toxicity (e.g. Dilantin has narrow TI)

What drugs are used in assisted suicide/ euthanasia

• Barbituate: Secobarbital

  • High dose (9 grams, PO)

• Note: Antiemetics given to prevent vomiting: e.g. metoclopramide

• Benzodiazepine: Diazepam

  • High dose

  • Note: Combined with 2 other drug classes (paralytic agents (e.g. Rocuronium) & anesthesia agents (e.g. Propofol))