Traumatic Brain Injury

Secondary Injury after Diffuse Axonal Injury

DAI also causes brain cells to die, which cause swelling in the brain. Increased pressure in the brain can cause decreased blood flow to the brain, as well as additional injury. The shearing can also release chemicals which can contribute to additional brain injury.

Contusions

a bruise on the brain, usually associated with swelling and some bleeding.

Traumatic brain injury (TBI)

an "acquired" insult to the brain, caused by external physical force that may produce a diminished or altered state of consciousness.

Oedema

describes swelling in the brain. Swelling can be minor or severe when associated with multiple contusions Diffuse brain swelling can cause compression or herniation.

Neurogenesis

the process of generating new neurons in the brain. mainly occurs during pre-natal development, and populates the growing brain. The ability of the brain to change and adapt with experience is known as neuroplasticity. With neuroplasticity comes neurogenesis. The development of new neurons continues during adulthood in two regions of the brain (hippocampus' dentate gyrus and sub ventricular region. The new neurons are produced by progenitor cells which are derived from stem cells in the brain. The stem cells renew the neurons continuously. This production of neurons involves three steps: 1. Asymmetric division of a stem cell producing one daughter stem cell and one that can develop into a neuron. 2. Migration of the newborn cell into it's place in the brain. 3. Maturation of the cells into a neuron.

Neurological and Neuropsychiatric effects of TBI

- Motor Impairments and Movement Disorders: Paresis (weakness) or plegia (paralysis), Spasticity (increased muscle tone and exaggerated reflexes), Ataxia (loss of muscle coordination), Post traumatic movement disorders manifest by either slowness or poverty of movement (hypokinesia) or by excessive involuntary movements (hyperkinesia), Two most common classifications of movement disorders are tremors and dystonia's (sustained muscle contractions which cause twisting or repetitive movements). - Balance and dizziness: Temporary or permanent deficits in static or dynamic balance. Dizziness is a common complaint in people with TBI of all severities. Vertigo (spinning sensation) is less common and typically caused by peripheral injury. Damage to brain stem and cerebellum is also central cause for balance problems. - Visual impairments: Can arise from orbital fractures, cranial neuropathies, brain stem damage or damage to subcortical or cortical regions involved with the visual system. Can cause blurred vision, binocular vision problems (diplopia (double vision), changes in depth perception, difficulty localizing objects in space), nystagmus, difficulty in visual tracking, and reading. - Headaches: temporary or chronic can occur following injuries to the neck, had or both. Typically resolves within 3 months. Conceptualised as chronic if > 3 or 6 months. Can be associated with depression and psychological distress. - Sexual dysfunction: Can involve changes in desire, drive, arousal and sexual functioning. Sexuality is influenced by physical, cognitive, emotional and social factors. Caused by damage to specific areas of brain, neurochemical changes relating to brain function, endocrine abnormalities, medication side effects, cognitive impairments, emotional problems, behavioural problems and interpersonal difficulties. - Fatigue and sleep problems: fatigue hard to access as highly subjective but highly debilitating. Commonly experienced as weakness, tiredness or exhaustion Fatigue can interfere with a persons cognitive functioning and day to day activities. Sleep disturbances are typically characterized by insomnia (difficulty initiating sleep), hypersomnia (excessive sleep)or disturbed sleep-wake cycles. Often fatigue and sleep problems co-occur with depression. - Depression and anxiety: Prevalence post TBI ranges fro 11% to 77 %. Most common in first 12 months, late onset depression has been reported 3 years post-injury. Unclear whether depression occurs as a biological consequence of TBI and/or psychological reaction to deficits and psychosocial problems related to injury. Post-injury anxiety disorders less common. Include generalized anxiety disorder (GAD), panic disorder, obsessive compulsive disorder (OCD), social phobia and post-traumatic stress disorder(PTSD). - Psychotic disorders: Post traumatic psychosis Causes, damage to left hemisphere particularly. Temporal and parietal lobes, increased severity of TBI, closed head injuries, predisposition to psychosis (having first degree relative with psychotic disorder), pre-morbid neurological pathology( prior brain injury, seizures, ADHD). - Personality Changes, Apathy and Motivation: Damage to specific regions of brain. For example: Frontal lobe damage can result in impulsivity, emotional liability, socially inappropriate behaviours, apathy, decreased spontaneity, lack of interest or emotional blunting. Damage to temporal lobes can result in hyper-irritability, aggressive outbursts or dysphoric mood states. Personality changes can also manifest as a reaction to the injury. Irritability, restlessness, low tolerance and apathy common. - Lack of awareness: Up to 45% who sustain moderate to severe TBI reported to have reduced awareness of medical, physical and/or cognitive deficits. People tend to underestimate the severity of cognitive and behavioural impairments when compared to rating by family members. Agnosia (impaired recognition of previously meaningful stimuli), anosognosia (lack of knowledge or awareness of cognitive, linguistic, sensory and motor deficits, Ansodiaphoria ( lack of concern for serious neurological impairments without denying their existence, denial of insight and lack of insight .

Closed Head Injury

A closed head injury is a trauma in which the brain is injured as a result of a blow to the head, or a sudden, violent motion that causes the brain to knock against the skull. Closed head injuries can be diffuse, meaning that they affect cells and tissues throughout the brain; or focal, meaning that the damage occurs in one area. Closed head injuries can range from mild to severe.

Neuropsychological Impairment following TBI

Cognitive impairment following TBI is highly individualized and difficult to predict and related to injury severity. Most cognitive deficits resolve within days to weeks post injury, with the vast majority having full recovery within the first year depending on severity those with severe TBI's are likely to have some degree of persisting impairment. Domains of cognition commonly associated with deficits post-TBI are; attention, concentration, working memory (immediate and delayed recall), information processing speed and memory. As the severity increases there is a greater likelihood of global cognitive deficits that include, motor skills, verbal and visual-spatial ability and reasoning skills. Neuropsychological evaluation is critical in monitoring the course of recovery or the effectiveness of rehabilitation.

Diffuse Axonal Injuries

Damage to the pathways (axons) that connect the different areas of the brain. Result of brain twisting and turning within skull at time of injury (sheared tissue). Affects more than one part of the brain. The neurons receive and transmit information in a relay where electrical impulses alternate with chemical messengers. The electrical impulses flow through nerve cell pathways along the axons and dendrites. Neuro-chemical transmitters leap the synaptic gaps between each neuron's axon and the other neurons with which an axon makes contact. Each neuron is its own miniature information center which decides to fire or not fire an electrical impulse depending on the thousand or so signals it is receiving every moment. In a diffuse axonal shear injury many of the nerve cell pathways (axons) may be torn apart or stretched. This can cause a loss of connection between brain cells and can lead to a breakdown of overall communication among neurons in the brain. Information processing may be disrupted. When the brain is being thrown at high speed in all kinds of directions, the nerve cells twist and turn, causing brain cells to shear and tear. As tissue slides over tissue, a shearing injury occurs. Nerve cells are damaged in this way, lose their ability to communicate with each other, so signals cannot pass through. Typically occur in specific brain regions such as grey and white matter interfaces of the cerebral cortex, the long fibres of internal capsule that carry information, crossing fibres that connect cerebral hemispheres (corpus collosum) and the upper brain stem.

Secondary Injury: Brain Herniation

Diffuse brain swelling can cause compression or a potentially deadly side effect of very high intracranial pressure. Swelling (odema) or a collection of blood (hematoma) can cause the brain to shift across structures within the skull or through natural openings. Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure.

Closed Brain Injury

Internal Pressure & Shearing: assaults, falls, accidents, abuse.

Skull fractures from head injuries

Linear usually thin and straight, and depressed which is when there is a dent in the skull.

Types of Cellular Death following TBI

Necrosis: form of traumatic cell death that results from acute cellular injury in response to severe mechanical or ischaemic/hypoxic tissue damage with excessive release of excitatory neurotransmitters and metabolic failure. Apoptosis: is the process of programmed cell death that may occur in multicellular organisms. Biochemical events lead to characteristic cell changes and death. The clinical relevance of apoptosis relates to the delayed onset of cellular deterioration.

Open Brain Injury

Penetrating Injuries: assaults, falls, accidents, abuse, surgery.

Primary and Secondary Mechanisms of TBI

Primary Insult: represents the direct mechanical damage occurring at the moment of impact. Primary damage involves axonal injury, vascular injury and haemorrhage Secondary Insult: represents consecutive pathological processes initiated at the moment of injury with delayed clinical presentation. Occurs hours, days or weeks post injury. Secondary damage arises from evolution of secondary systematic processes: including ischemia, energy failure and cell death cascades, swelling in the brain (odema) and inflammation.

How does TBI Occur?

Traumatic brain injury (TBI) generally results from mechanical impact or acceleration-deceleration insults that cause skull fractures, compression of cerebral tissues, and tearing of white and grey matter and subsequent haemorrhage.

Secondary brain Injury: Intracranial Pressure

caused by a) the added mass of epidural, subdural, and intracranial hematomas and b) cerebral odema which develops around large contusions, and from diffuse vascular injury. Any increase in intracranial mass will first displace CSF into the spinal subarachnoid space. An increase of intracranial pressure above 40-50 mm Hg will collapse brain capillaries resulting in global ischemia.

Secondary Brain Injury : Ischemia

caused by restriction of blood flow to brain. Results in poor oxygen supply or cerebral hypoxia and cellular death Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis which influence blood flow to the brain. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue.

Coup/contrecoup Injury

follows a classic lesion pattern: A coup injury occurs at initial the site of impact with an object, a contre-coup injury occurs on the side opposite the area that was impacted. Causes the brain to first slam into one side of the skull wall, then bounces off that wall and slam into the wall on the opposite side of the skull.

Hematoma

is a accumulation of blood in a specific location in the brain caused by a break in a blood vessel. When damage to the brain causes a large bleed, it may form a pocket of blood, called a hematoma. There are three different types of hematomas, depending on where the pocket of blood is found: Epidural hematoma: This is a collection of blood between the skull and the top lining of the brain, or Dura mater. Epidural haematomas can be quite severe and cause loss of consciousness within hours of the injury. Subdural hematoma: This is a collection of blood between the Dura mater and the arachnoid. Subdural haematomas can form slowly over time; sometime taking days before there are any symptoms, which may include increasing headaches and confusion. Intracerebral hematoma: A collection of blood deep within the brain. Symptoms will depend on where in the brain the bleeding happens. For example if it occurs in an area that controls speech, a person may become unable to communicate . If it happens in an area that controls movement, they may become unable to move their arm or leg.

Secondary brain injury

is an indirect result of trauma. Results from processes initiated by the trauma. Can occur hours, days and even weeks post injury. Can result from complications of injury. Cerebral swelling/bleeding days/weeks post-injury. These include ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); hypotension (low blood pressure); cerebral swelling of the brain; changes in the blood flow to the brain; and raised intracranial pressure If intracranial pressure gets too high, it can lead to deadly brain herniation, in which parts of the brain are squeezed past structures in the skull. Metabolic cascades. Hypoxia and hypotension greatest threat to functional outcome in brain injury.

Neuroplasticity

is the brain's capacity to change and adapt. Neural plasticity "regenerative processes to regain functionality". Refers to the physiological changes in the brain that happen as the result of our interactions with our environment. From the time the brain begins to develop in utero until the day we die, the connections among the cells in our brains reorganize in response to our changing needs. This dynamic process allows us to learn from and adapt to different experiences. Three phases: 1. Cell repair. 2. Existing neural pathways may change. 3. New neural networks can become established. Basis for cognitive and physical rehabilitation practices. Part of rehabilitation is aimed at trying to rebuild connections among the nerve cells — or neurons. This "re-wiring" of the brain can make it possible for a function previously managed by a damaged area to be taken over by another undamaged area. The connections among the cells are infinitely receptive to this type of change and expansion.

Secondary brain Injury: Cerebral Hypoxia

reduced oxygen supply in the brain. Hypoxia can rapidly cause severe brain damage. Some brain cells start dying less than 5 minutes after their oxygen supply disappears. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brainstem reflexes, and cellular death. brain requires approximately 3.3 ml of oxygenated blood per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain's oxygen needs then no symptoms will result. If blood flow cannot be increased symptoms of cerebral hypoxia will begin to appear.

Haemorrhage

represents bleeding in or around the brain. Haemorrhages within the brain are caused by damage to an artery or vein Increased symptoms can present 2-4 days post trauma Bleeding and swelling injures the internal neural network and is often pervasive and not just localized at the site of initial impact. Some individuals may be lucid for an interval following an impact to the head. They will then experience a deteriorating level of consciousness. This can be indicative of a head injury involving bleeding.