Pathophysiology (M9)

Neurological Disorders

Consciousness 

awarness of self/enviorment 

1. arousal (wakefulness) 

2. content/cog 

Arousal 

= wakeful/alert

reticular activating system (RAS) → starts @ brain stem, network diffuses across brain 

• loss of arousal: injury to RAS/both hemispheres (h: same time) 

• if one hem damaged: arousal not lost 

Content & Cognition

cog functions, involved in awarness

1. selective attention: selectivley pay attention

2. memory

3. executive attention: maintain attention, remember instructions, etc.

Level of Consciousness (LOC) → both arousal & cognition

Colin Stabs Old Dentist Crazily

• Coma (not arousable)

• Stupor (arousable to pain)

• Obtundation (low arousal, sleepy)

• Delirium (restless, hallucinations)

• Confusion (disoriented, fuzzy thinking, poor responses to stim)

assessed by glasgow coma scale

Glasglow Coma Scale

score indicates LOC, each trait scored, based on:

1. eye opening

2. verbal response

3. motor response

3 is lowest score = brain dead

Brain Dead

= no recovery possible & brain cant maintain homeostasis

criteria:

• established cause

• absence of motor/brainstem reflexes 

• apnea test (breath wo vent) 

• lack of other cause (ex. drugs) 

Cerebral Death

• irreversible coma 

• brain stem maintains homeostasis 

• cant respond significantly to enviorment 

Persistent Vegatative State

• complete unawarness

• sleep wake cycle present

• brain stem reflexes intact (bowel/bladder leak)

Minimally Conscious State

• follow simple comands

• may enter after persistent veg state

Locked in Syndrome 

• paralysis of voluntary mucles, EXCEPT eye movement 

• fully concious 

• cant communicate w speech/body 

Respiratory Responses: Cheyne-Stokes breathing

• higher brain injury 

• alternating periods of apnea & tachypnea 

• response of ↑ CO2 in blood 

Respiratory Responses: Neurogenic Hyperventilation

• injury to midbrain

• more than 40 breaths per min 

• insp/exp centers continously stimulated 

Pupillary Reflexes & Eye Movement

pupil change: light exposure → fixed/dilated/pinpoint/unequal, determines location/extent of brain damage 

• ex. damage/pressure on oculomotor nerve to one eye → causes other pupil to be non responsive (blown) 

Oculocephalic Reflex/Doll’s Eye Response 

• eye movement opposite from head movement 

• abnorm: eyes follow head/independent movement (comatose patients) 

Abnormal Body Responses in Extremities: Decorticate Posture

• upper extremities flexed @ elbows (held close to body) 

• lower extremities = internally rotated/extended 

• cerebral hemisphere damage 

cor = core, arms pulled to core 

Abnormal Body Responses in Extremities: Decerebrate Posture

• clenched jaw/extended neck 

• limbs rigidly extended 

• brain stem lesions 

lots of e’s = e’s in position (w hands/feet)

Seizure Disorders & Types 

= sudden/explosive discharge of cerebral neurons (temp change in brain func → altered arousal)

types-

focal: begins in 1 side of brain

generalized: both sides involved

• mild: starring spells, no body shakes, maybe unnoticed

• major: convulsions = jerky, muscle contaction/relaxation

causes: cerebral lesions/trauma, epilepsy

Generalized Tonic-Clonic Seizure

• Aura: warning sign before seizure begins, abnormal sensations/confusion

• Tonic: sudden/temporary stiffening of muscles 

• Clonic: jerky involuntary movements 

Data Processing Deficits: Agnosia? Hemineglect?

problems recognizing/processing sensory info:

• A: fail to recognize form/nature of objects, affects one sense (ex. recognize saftey pin w touch, not when looking)

• H: inable to react to stimuli from contralateral side (opp to damage) → may not use those limbs/wont visually track 

Data Processing Deficits: Dysphasia? Aphasia?

D: understanding/use of symbols (written/verbal) disturbed/lost, dysfunction in L cerebral hemisphere (ex. stroke/trauma) 

A: inable to communicate (interchangeable w D)

• brocas: damage to brain responsible for language production (b= broken words) 

• wernickes: damage to area responsible for comprehension (w= what?, cant understand) 

Increased Intracranial Pressure (IICP)

• from anything taking up volume in brain (ex. tumour/excess CSF) 

• adjust to ↑ pressure: needs reduction in cranial content → includes blood/CSF/tissue volume (Monro-Kellie hypothesis) 

• brain intially adujsts through loss of CSF → doesnt fix = cerebral blood volume/flow altered 

Stages of Intracranial Hypertension: Stage 1

(asymp)

to ↓ ICP

1. CSF displaced into spinal subarachnoid space (↑ reabsorp)

2. external compression of venous system (limited blood, cant buffer as much, ↑ CO2 causes dilation)

Stages of Intracranial Hypertension: Stage 2

• further swelling ↑ ICP 

• ↓ in brain tissue perfusion & poor oxygenation (confused/restless)

• vasomotor center response: systemic constriction, ↑ systemic blood pressure = Cushings Reflex 

Stages of Intracranial Hypertension: Stage 3

• hypoxia/hypercapnia of brain tissue 

• rapid detrioration: ↓ arousal, small slugish pupils  

• compensatory mechanisms used, dramatic ↑ in ICP 

Stages of Intracranial Hypertension: Stage 4

• brain tissue shifts (heniates) → to compartment of lower pressure

• ICP = systolic arterial pressure

• cerebral flow ceases → death 

Causes of IICP: Cerebral Edema

• ↑ fluid content → ↑ brain tissue vol 

• after: trauma, tumour, ischemia, etc

• distorts vessles, displaces brain tissues, herniation

• 2 types 

Vasogenic edema? Cytotoxic? 

V: 

• ↑ perm of blood brain barrier

• plasma protiens leak out of capillaries = ↑ water content of tissue

• white matter 

C:

• toxins/hypoxia = failure of transport mech of cells

• ↑ na/water in cell

• gray matter

Causes of IICP: Hydrocephalus, 2 types?

= excess fluid in ventricles/subarachnoid space

from excessive CSF production/little reabsorp 

2 types: 

• Noncommunicating: obstruction prevents  CSF from reacing/absorbed by arachnoid vili

• Communicating: cant reabsorp cuz of reduced #/scarring of arachnoid vili, overproduction of CSF 

acute onset → ICP

Altered Neuromotor Function: Alterations in Muscle Tone

disruptions in motor NS → dysfunction in 1 of 3 traits: 

muscle tone: norm state of mucle tension (controlled movement/posture) 

cause: injury to part of motor pathway 

• hypertonia: rigid, injury to uper motor neurons, ↑ tone (inhibitory effect of brain on spinal cord reflex is removed) 

• hypotonia:  flacid, injury to lower MN (LMN), ↓ tone

Altered Neuromotor Function: Alterations in movement

• Paresis: weak 

• Paralysis: loss of motor neuron function, muscle group cant overcome gravity, in upper/lower motor neurons, diff classifications 

• Hyperkinesis: excessive movements, phys/chem causes 

Paralysis Types

• Monoplegia: single limb

• Hemiplegia: one side of body 

• Tetraplegia/Quadriplegia: all 4 limbs 

• Paraplegia: lower body 

Disorders of Posture 

inequality of tone in muscle groups → loss of norm postural reflexes 

• decorticate & decerebrate

• basal ganglion posture: stooped, hyperflexed w narrow, short stepped gait

Disorders of Gait? Expression? 

Gait: 

• spastic: shuffling gait w extended leg & held stiff

• scissor: stiff legs, swing around & cross in front

Expression:

• hypermimesis: inappropriate laugh/cry

• dyspraxia/apraxia: cant perform tasks needing learned motoer skills → issue w muscle use, not comprehension 

Brain Trauma: closed v open? primary v. secondary? 

caused by closed (blunt) or open (penetrating) trauma 

• closed: dura intact, can result in focal brain injuries (1 area)/diffuse axonal injury (more than 1 area) 

• open: break in dura, exposes cranial contents to enviroment 

2 categories: 

• prim: damage from impact 

• sec: damage after swelling/infection/hypoxia 

Primary Brain Injury: Focal Brain Injury 

impact, 2 types: focal & diffuse 

• specific, observable brain lesions in precise location 

Focal Brain Injury: Contusions (2 types)

=blood leaking from injured blood vessels

Coup: impact against object, direct trauma to brain @ point of impact 

Contrecoup: rebound of brain against opp side of skull, impact injury on brain area opp to object 

• both occur in continous motion 

• edema around area w infarction/necrosis/hemorrhage, peak: 18-36h after 

Contusions- events

• immediate loss of consciousness 

• loss of reflexes 

• brief: no resp/brachycardia, ↓ bp 

• vita signs stabilize in few secs 

• may have residual effects 

Focal Brain Injury: Hematoma? Extradural 

bleeding in/beside brain, from trauma, produces area filled w blood

• injury (fracuture) causes bleeding b/w dura & skull (arterial bleed) 

• delay before symptoms (lucid period → 2/3 hours before/w signs & event → deteroriation as pressure ↑)

• recovery good if hematoma removed (eyes: ipsilateral pupil dilation/contralteral hemiparesis)

Focal Brain Injury: Subdural Hematoma

• venous, ↓ pressurre, slow bleeding

• acute/post trauma: devlop within hours

• chronic/other condition: devlops over weeks/months

Focal Brain Injury: Intracerbral Hematoma

• bleeding in brain

• penetrating injury/shearing → trauma to small vessels

• delayed (3-10 days later)

Diffuse Brain Injury

(diffuse axonal injury - DAI)

• widespread neual axon brain damage 

• from: shaking/rotating/twisting (seen w microscope) 

• slow info proccesing 

• spectrum, depends on severity (best: concussion) 

Diffuse Brain Injury: Mild? Classic Cerebral? Mild DAI?

MC: no loss of consciousness, CSF pressure ↑, confusion for mins, retrograde amnesia 
CC: loss of conciousness (up to 6hr), confused for hours, headache/nausea, retrograde
MD: (6-24hr coma) decerebrate/decorticate posture, extended periods of stupor/restless 

Diffuse Brain Injury: Moderate v. Severe DAI?

M: (more than 24h), d/d posture, unconscious for days/weeks, wake = perm deficit in mem/reason/language 

S: (emerge from coma in first 3 months), result: compromised cordinated movement, verbal/written com, learn/reason 

Secondary Brain Trauma 

• indirect result of prim trauma 

• mech: cereral edema, IICP, ↓ perfusion, ischemia, herniation 

• damage: hours/days after prim trauma 

Cerebrovascular Disorders

C disease: abnormality of brain by pathologic process in blood vessel (ex. rupture/lesions) →  causing ischemia/hemorrhage 

lead to: cerebrovascualr accident (CVA) → STROKE 

• acute focal neurologival deficit from vascular disorder, injures brain tissue 

• 2 types: ischemic & hemorrhagic 

Ischemic Stroke: Thrombotic (large vessel) 

• blockage by thrombi in large arteries in brain (devlop through athero) 

• causes acute ischemia 

• affects cerebral cortex (symptoms: aphasia/neglect/visual field defects)

• occur at rest, older 

Ischemic Stroke: Lacunar (small vessel) 

• small infarction, deep in brain (internal capsule/basal ganglia/stem) 

• from: emboli/hemorrhage/vasospasm

• manifest: sensory/motor hemoplegia, dysarthria 

• risks: chronic hyperten/diabetes 

Ischemic Stroke: Embolic