Week 2: Stroke, TBI and ND conditions

Traumatic Brain Injury (TBI)

•   Caused by external forces

  •   Penetrating objects (projectiles e.g. gunshot)

  • Blunt/ direct impact (motor veichal accident, falls, sport)

  • Rapid acceleration and deceleration (motor veihcal accident, shaken baby syndrome)

  •   Bast explosions

• Symptoms include

  • loss of memory prior to/after event

  • Neurological impairment (weakness, paralysis, sensory loss, visual disturbances)

  • Change in mental state (disorientation, confusion, slowed thinking)

  • Evidence of damae to brain (external/neurimaging)

Non-traumatic brain injuries (acquired)

Caused by internal factors

• Haemorrhahypoprofusion(e.g. anurysm)

• Occlusion/ blockage/ lacj of blood (ischaemia)

  Thrombotic (thrombus/clot in artery)

  Embolic (embolus travels and lodges in artery)

  Systemic hypoprofusion (decreased blood flow due to bleeding, failure of heart to pump blood)

Stroke/ cerebraovascular accident (CVA)

Lack of blood supply (any mechanism)= lack of 02, nutrients to the area, inability to remove wastes

• Begins process of cell necrosis (death)

• Longer lack of blood= ^ extent of cell death

• Larger area not supplies= ^ area of cell death

• 2 major types of stroke: Haemorrhagic and ischaemic

Ischaemic stroke

Occlusion/ blockage/ clot

2 subtypes

• Thrombolic

  • Most common

  • Thrombus/clot builds in artery within brain

  • Often due to atherosclerosis (plaque build up= gradual narrowing/ blockages)

• Embolic

  • Embolus travels from elsewhere in the body and lodges in artery in brain

Location of blockage, how long blocked for impacts size/impact (extent of cell death)

Haemorrhagic stroke

     Bleeding into brain tissue

Subtypes naed by location in relation to meninges

• Epidural haematoma- between skull and dura mater

• Subdural haematoma- between dura and arachnoid mater

• Subarachnoid haemorrhage- between arachnoid and pia mater

• Intracerebral haemorrhage- within cerebrum

  • Commonly from hypertension or burst aneurysm

  • Can also get from TBI (though is a different mechanism)

  • Most fatal with widespread impact as difficult to stop the bleed

Common ABI mechanisms

• Stroke/ cerebrovascular accident

• Toxins

• Infection

• Tumours

• Hypoxia (lack of 02)

Primary and secondary injuries

-              Contusions (bruising)

-              Lacerations (cuts)

-              Compression (to spinal cord)

-              Diffuse axonal injury (tearing of axons)

-              Haemorrhage (bleeding)

-              Ischaemia (occlusions/lack of blood)

-              Necrosis (cell death)

-              Oedema (swelling)- ^ intercranial pressure (hydrocephalus)

-              Haematoma in meninges (pooling of blood)

-              Risk of infection

Blood supply to the brain

• Blood arrives through 2 major arteries

• Internal carotid artery

  •   Circulation to anterior parts of brain

  • Splits into anterior and middle cerebral arteries

  • Supplies frontal, temporal, parietal lobes and parts of corpus callosum, basal ganglia

• Vertebral artery

  •   Posterior circulation

  • Supplies occipital lobe, parts of temporal lobe, hypothalamus, thalamus, internal capsule, basal ganglia, cerebellum, brainstem

•     These arteries join together to form circle of Willis

Stroke diagnosis

•   1 way of describing- by arteries impacted (either haemorrhage or blockage)

• Major arteries we’re focusing on

  • Middle cerebral artery (MCA) (most common)

  • Anterior cerebral artery (ACA)

  • Posterior cerebral artery (PCA)

  •   Posterior circulation arteries

•   Lacunar stroke- blockage to small artery deep within the brain (no widespread damage)

Total atrial circulation syndrome Infarct (TACI)

• Large cortical stroke affecting both MCA and ACA territories

• Must have:

  • Unilateral motor/ sensory deficit (hemiplegia, hemianesthesia)

  • Homonymous hemianopia

  • Higher cortical dysfunction (e.g. aphasia, neglect)

Partial atrial circulation syndrome Infarct (PACI)

• Smaller cortical stroke affecting part of MCA and ACA territory

• Must have 2/3 or isolated higher cortical dysfunction:

  • Unilateral motor/ sensory deficit (hemiplegia, hemianesthesia)

  • Homonymous hemianopia

  • Higher cortical dysfunction (e.g. aphasia, neglect)

Types of TBI

• Closed v open

  • Penetrating or purely internal

  • Open= risk of infection

• Focal v diffuse

  • Focal= more localised/ specific to site of impact

    • contusions, coup-contrecoup, lacerations, haematomas

  • Diffuse= more widespread/global impact

    • Traumatic/ diffuse axonal injury, hypoxias

Haematomas

• Bleeding into brain tissue (haemorrhage) that pools = haematomas

•   Subtypes are named by their location in relation to the meninges

  • Epidural haematoma – between skull and dura mater

  •   Subdural  haematoma – between dura and arachnoid mater

  • Subarachnoid haemorrhage – between arachnoid and pia mater

  • Intracerebral haemorrhage – within the cerebrum

•   In TBI, haematomas often secondary to contusions/ lacerations

•    Therefore occur via similar mechanisms (MVA, fall, penetrating injury)

•    If bleeding cannot be stopped, becomes a global injury, due to loss of blood AND increased pressure

Neuroplasticity

• The brain has the capacity to reorganise itself by forming new neural connections – known as neuroplasticity (basis for rehab)

• This means that new neural connections can form and replace damaged connections – i.e., damage from a stroke or TBI is not necessarily permanent/fixed

• “Synaptic pruning” – unhelpful connections are deleted and new pathways are strengthened

  Knowledge of Neuroplasticity help recovery by:

• Facilitating early initiation of therapy

• Refraining from excessively vigorous motor function rehab too soon post-injury

• Using task-specific training in rehabilitation

Neuroplasticity depends on

• Age (harder for adults than kids)

• Severity of neurological damage

• Pre ABI health

Parkinsons

• Caused by damage to the substantia nigra of the basal ganglia, resulting in a lack of dopamine.

• Input to the corpus striatum (structures of the basal ganglia), thalamus and motor cortex becomes impaired

• Considered to predominantly be a movement disorder, due to the key roles of the basal ganglia in motor control

• However we also know the basal ganglia has functions beyond motor control

4 Clinical markers of Parkinsons

• Tremor (not as bad early on-need t be careful as can also be caused by medications)

• Rigidity

• Bradykinesthesia (slowness of movement)

• Postural instability (later stage symptom)

• Diagnosis requires bradykinesia + rigidity and/or tremor

Presentation associated with basal ganglia damage (seen in PD)

• Leadpipe rigidity: Increase in muscle tone

• Cogwheel rigidity: Leadpipe rigidity +tremor= jerky resistance to passive movements (muscles shift between tensing and relaxing)

• Bradykinesia: Slowness of movement

• Gait festination: Rapid, small steps that attempts to maintain centre of gravity while the trunk leans forward (due to postural instability)

• ‘Freezing’: Temporary involuntary inability to move (believed to be linked to balance disruption/change of movement); particularly in doorways

• Tremor: involuntary oscillating movements due to abnormal opposing muscle contractions. Can be essential (tremor upon movement) or resting (tremor at rest)

• Tics: Repetitive, brief, rapid, involuntary, purposeless movements/behaviours. Range of presentations; motor tics (e.g. head jerks); phonic tics (throat clear, grunt); involuntary repetition of words (e.g. echolalia)

Multiple sclerosis

• A progressive neurological condition

• Auto-immune disease that causes demyelination of axons throughout the brain and spinal cord (and particularly the optic nerves), impacting nerve transmission

• Remember from Patho, immune response is our body’s way of depending itself

  • In auto-immune, immune system mistakenly attacks your own body (in this case, the myelin specifically)

  • Can occur in cycles of flare-up)

Clinical courses of MS

• 3 clinical courses whereby the condition either gradually declines, or is experienced in courses

• Experience is influenced by which course they are experiencing and where they currently sit on the course

  • Relapsing- remitting

  • Secondary progressive

  •   Primary-progressive

Relapsing-remitting MS (RRMS)

• Most common

• Characterised by cycles of attacks followed by partial or full recovery

Secondary progressive MS (SPMS)

• Relapsing-remitting presentation that then becomes steadily progressive (i.e. steady decline in function). May still experience some cycles of attacks followed by partial recoveries (as per RR)

• Of those who begin with a RR presentation, 50% will move to secondary progressive within 10 years; and 90% within 25 years

Primary profressive MS (PGMS)

• Steady progression (i.e. functional decline) from onset, generally without remission/recovery (unlike RR)

• 15% of people with MS will experience this clinical course from the outset

Key symptoms of MS

• Symptoms very depending on where CNS demylination is taking place and to what degree

• Consists of 5 major issues

  • Motor control

  • Fatigue

  • Other neurological symptoms (often vision)

  • Continence issues (often starts at night and gets worse)

  • Neuropsychological symptoms (mental health issues)

Middle cerebral artery (MCA)

• Supplies lateral, frontal, parietal, and temporal lobes

• Impacts: motor/sensory deficits (face and arm), aphasia, neglect

Anterior cerebral artery (ACA)

• Medial, frontal and pariatal lobes supplied

• Impacts: Lower limb weakness, apathy, impaired initiation

Posterior cerebral artery (PCA)

• Occupital lobe, inferior temporal lobes supplied

• Impacts: visual deficits, reading difficulty, memory issues

Brain injury impacts

• Motor (voluntary motor control; motor planning; coordination, posture, tone)

• Sensory

• Language

• Cognition (Orientation, attention, memory; executive function)

• Emotion/personality

• Vision

• Perception

TBI: Contusion

• Localised trauma, causing bleeding and swelling in the brain – known as brain tissue bruising

• Essentially same mechanism as a haemorrhagic stroke – except forces creates rupturing of blood vessels

• Can also cause the chhaematomatween the ventricles that have cerebrospinal fluid to be blocked due to the swollen brain tissue/haematoma, which is very serious (hydrocephalus)

Coup-contrecoup injury

• Associated with falls, motor vehicle accidents (MVA)

• Brain movement due to trauma forces make it hit the inside of skull on side, and then opposing side

• Creates contusion at site of impact (coup), plus the opposite side of impact (contre-coup) – i.e. double contusion

• Commonly impacts frontal and occipital areas

Lacerations

• Laceration means cut/tear

• Tears result from penetrating object (i.e. via an open TBI) or from the skull itself, often when fractured

• Creates tearing of brain tissue and blood vessels, and therefore subsequent bleeding (and increased pressure, etc

• Often co-occurs with contusions, and commonly via similar mechanisms (MVA, falls), as well as via penetration injuries (e.g. gunshot)

Diffuse axonal injury

• Product of acceleration-deceleration, which creates opposing forces that try to simultaneously move the brain backwards and forwards – e.g. via MVA or shaken baby syndrome

• These forces create stretching and ultimately ‘shearing’ (tearing) of axons – i.e. separates grey matter/cell bodies from white matter/axons – meaning no messages can be sent

• Can impact cerebral hemisphere areas, corpus callosum, brainstem

• Often devastating – commonly results in coma, major cause of persistent vegetative state

Increased intracranial pressure

• An increase of pressure within the skull

• occurs due to swelling/ increase in volume of brain tissue, CSF or intercranial blood (haemorrhage, haematoma, obstruction of CSF or infections creating inflammation (meningitis)

• Can result in seizures, furthur neurological damage, stroke or even death

• Pressure needs to be relieved quickly- can occur via medication, draining of excess fluids (CSF or blood) or performing craniotomy (removing part of the skull)

Hypoxic brain injury

• Reduced 02 in brain, damage within 3-4mins

• Causes can be traumatic or ‘non-traumatic’ (near drowning, drug use)

• Damage depends on length of time, partial or complete 02 deprevation, coupled with other damages

• Diffuse injury- widespread across the brain

Sub-arachnoid haemorrhage

• Bleed at the surface of the brain in space between arachnoid and brain surface

• Ruptured blood vessels due to: trauma, aneurysm, arteriovenous malformation

• Causes pressure to build up (can be life threatening)

• Impact influenced by size and location of the bleed, and time until treatment

Cerebrospinal fluid

• Fluid that circulates in the ventricles (cavities/spaces), subarachnoid space and spinal column

• Purpose: regulates extracellular fluid contents in CNS (including electrolytes and distribution/removal of metabolic products)

• Protects and supports brain and spinal cord (shock absorbtion)

• Blockage that inhibits drainage/flow or excess CFS produced, intracranial pressure is increased --> hydrocephalus

Meninges (cerebral and spinal)

• Dura mater: tough, thick and attached to inner surface of skull

• Arachnoid mater: spider web like

• Pia mater: sits directly overt brain