Brain stem - lower extension of brain where it connects to the spinal cord. Neurological function is located in the brain stem include those necessary for survival (breathing, digestion, heart rate, blood pressure) and for arousal (being awake and alert). Most cranial nerves come from brain stem. It is pathway for all fibre tracts passing up and down from peripheral nerves and spinal cord to the highest parts of the brain.
Cerebellum - portion of brain (located at back) that helps co-ordinate movement (balance and muscle co-ordination). Damage may result in ataxia, which is a problem of muscle co-ordination. This can interfere with a person's ability to walk, talk, eat and to perform other self-care tasks.
Frontal lobe - front part of brain involved with planning, organising, problem solving, selective attention, personality and a variety of "higher cognitive functions" including behaviour and emotions. The anterior portion of the frontal lobe is called the prefrontal cortex. Very important for the "higher cognitive functions" and the determination of the personality. The posterior (back) of the frontal lobe consists of the premotor and motor areas. Nerve cells that produce movement are located in the motor areas. The premotor areas serve to modify movements. The frontal lobe is divided from the parietal lobe by the central culcus.
Occipital lobe - region in back of brain which processes visual information. This lobe is responsible for visual reception and also association areas that help in visual recognition of shapes and colours. Damage to this lobe can cause visual deficits.
Parietal lobe - one of the two parietal lobes of the brain is located behind the frontal lobe at top of brain. Parietal lobe (right) damage can cause visuo-spatial deficits (difficulty finding way around new - or even familiar - places). Parietal lobe (left) - damage can result in disruption of ability to understand spoken and/or written language The parietal lobes contain primary sensory cortex which controls sensation (touch, pressure). Behind primary sensory cortex is a large association area that controls fine sensation (judgment of texture, weight, size, shape).
Temporal lobe - two temporal lobes one on each side of the brain located at about ear level. These lobes allow person to tell one smell from another and one sound from another. Also help in sorting new information and are believed to be responsible for short-term memory. Right lobe is mainly visual memory (pictures and faces) Left lobe mainly verbal memory (words and names).
Many causes of coma - most frequent cause is due to trauma or injury to the brain as a result of accident, fall or blow to head. Additionally, severe injury as occurs in near-drowning. Brain is injured as a result of insufficient oxygen. Severe uncontrolled diabetes. Hepatic (liver) coma and uremic (or kidney) coma. May result from infection of brain (encephalitis) or brain tumours. Coma may result from ICP (as with severe hydrocephalus). Shunting operations used to relieve this pressure. Stroke can produce profound coma as with brain tumour indirectly causing raised ICP. Because of advances in technology (MRI and CAT scan, the ICP monitor and shunt) brain injury in general more likely to have a positive outcome than several years ago. Important function is prevention of further damage. Brain injury causes swelling. This causes compression in skull case which in turn decreases blood flow and oxygen to parts of brain which in turn causes more swelling. The goal of the neurosurgeon is to break or diminish this cycle. This can be done by removing the haematomas (blood clots) that are pressing on brain and surgically repairing damaged blood vessels to stop further bleeding. This gives brain more room, increased blood flow and helps stem cycle of compression and swelling.
In severe cases portions of brain that are damaged beyond recovery may be removed to increase chances of recovery for the healthy portions of brain. Also responsible for inserting monitoring devices for ICP. Measure pressure within brain and alert medical team to increases in pressure allowing them to intervene when dangerous levels are reached. A shunt or ventricular drain may be used to drain off excess fluids or surgical intervention may be called for. Overall goal is to maintain blood flow and oxygen to all parts of brain, minimising damage and increasing prospect of survival. According to the Rancho Los Amigos Scale, level I is the only pertinent one. It is defined as appearing to be in a deep sleep and unresponsive to stimuli. There are seven other levels lessening in severity to level VIII: Purposeful-Appropriate. This is being alert and oriented and able to recall and integrate past and recent events. Learn new activities and continue in home and living skills, though deficits in stress tolerance, judgment, abstract reasoning, social, emotional and intellectual capacities may persist. These levels can be regarded as "emerging" from coma. The improvement from level I.
Coma is only produced when there is dysfunction of both cerebral hemispheres. This can be due to damage involving both hemispheres or can be secondary to marked metabolic disturbances which produce widespread cortical dysfunction. Commonly, coma is due to dysfunction of the reticular activating system (RAS). The RAS cells originate in the lower pons and extend to the thalamus. They synapse there and project to the entire cortex. The RAS can be viewed as an "energiser" of the cortex. The RAS turns on the cortex when we awaken (decrease in RAS activity) and turns off the cortex when we drift into sleep. Structural damage to the RAS either from intrinsic brain stem damage (stroke, bleed) or from secondary compression of the RAS due to mass effects from hemisphere lesions (herniation syndromes) will produce profound coma. Similarly, CNS depressant drugs or severe metabolic disturbances can disrupt RAS function and produce coma. Problem is to determine whether coma is from bilateral cortical damage or from RAS compromise and then to remedy the underlying cause whether it be mass effect, metabolic or toxin.
Physical diagnosis is critical since history is often lacking in the comatose patient. Physical examination fairly simple in the comatose patient essentially four systems need to be examined. Examination should be matched with regard to metabolic or structural damage. Metabolic processes should have non-focal examinations. There will be no evidence of focal disease as manifested by hemiparesis or cranial nerve dysfunction. If structural damage there may be focal signs and the examiner must determine whether these are due to hemispheric or brain stem disease. Remember there must be bilateral cortical dysfunction or compromise of the RAS to produce coma. Prolonged period of unconsciousness. This is a lack of appreciation of (or no reaction to) stimulus.
Coma differs from sleep in that one cannot be aroused from coma. Involves two concepts - reactivity and perceptivity. Reactivity refers to the innate (or inborn) functions of the brain (telereceptors of eyes and ears), the nocireceptors (responses to pain), the arousal reaction (wakefulness) and the orienting response (turning one's head toward the source of sound o r movement). Could also refer to these as reflexive movements. Perceptivity refers to responses of the nervous system to stimuli, which have been learned or acquired (language, communication skills, individual methods of movement such as gestures). Also refers to less complex learned or acquired reactions such as flinching when threatened. Also think of these as conscious movements. A person in coma does not exhibit reactivity or perceptivity. Cannot be aroused by calling name or in response to pain. As emerge from coma may begin to react to certain stimuli. To regain "consciousness" reactivity and perceptivity must both be present. These two elements are necessary for a state of awareness.
Often many of elements of perceptivity must be relearned, such as speech, self-care. Person in coma may exhibit movement or make sounds and experience agitation. Coma patient may be restrained to keep from removing or dislodging IV tubes. Progress of coma is measured by patient's increasing awareness of external stimuli. Many levels of coma which patient will p ass through as functionality increases. Coma may sometimes is induced by chemical means to aid medical treatment and recovery. Some patients remember very distinctly events while in coma. In brain injury "waking up" or emerging is a slow process. Eyes open and wake/sleep cycles - sleep being longest. As wake cycle gets longer movement begins to occur, then speech, then purposeful movement, purposeful speech (asking questions). Arms an d legs first to move then head from side to side. Speech begins with moaning, then mumbling. No two brain injuries are alike.
Sometimes, coma patient may exhibit behaviours which mimic conscious behaviours - perhaps turn head toward sound. This may or may not be purposeful movement. Recovery from brain injury takes time. Even in the event of "mild" brain injury there may be no loss of consciousness but may experience long-term problems with memory, fatigue, concentration, anger, dizziness. These problems may never be resolved. Even if patient recovers quickly may take years to fully understand extent of injuries. May have deficits not obvious until faced with a new or different situation or environment - "subtle" deficits.
Nearly all tissues in body swell when traumatised. Also require more oxygen to heal. The brain rests inside bone case, so when swells experiences more trauma. The more the damage the more oxygen required and the more it swells. The swelling caused by leakage from blood vessels so when swells and constrained from doing so, leads to ICP (intracranial pressure). This rise in pressure rapidly equals arterial pressure affecting blood flow in brain. This diffuse pressure, which decreases blood flow, affects ability of cells to metabolise properly and cells are unable to eliminate the toxins that accumulate. This leads to a spiral effect that kills brain injured people who don't get prompt attention. Survival rate has greatly increased by learning how to break this cycle. Still early stages but most significant factor is use of monitoring devices. In response to trauma, changes in brain require monitoring to prevent further damage.
Size frequently increases after severe head injury - brain swelling. Caused by increase in amount of blood to the brain. Later may collect water in the brain - brain oedema (accumulation of fluid). Both brain swelling and oedema result in excessive pressure - ICP. Treatment can be difficult. Very strong medications are administered - those that draw fluid back out of brain and into blood vessels may be useful. Also, those that decrease the metabolic requirements of brain. Other medications can increase blood flow into brain and can help diminish the spiral effect caused by brain swelling. In some cases removal of small amounts of fluid from brain or surgery may be beneficial ("shunt").
Rancho Los Amigos Scale
Most helpful in assessing the patient in the first weeks or months following injury since it doesn't require co-operation from patient. These levels are based on observations of patient's response to external stimuli. Provide descriptive guidelines of various stages of brain injury patient will experience as progress through recovery. Just as every brain injury is unique so is rate of recovery. Can't predict speed of progress from level to level or at which level patient will reach plateau, which is a temporary or permanent levelling off in recovery process. An understanding of the eight levels provides insight into the progression through recovery and rehabilitation.
I. No response. Patient appears to be in deep sleep and is unresponsive to stimuli.
II. Generalised response. Patient reacts inconsistently and non-purposefully to stimuli in a non-specific manner. Reflexes are limited and often the same, regardless of stimuli presented.
III. Localised response. Patient responses are specific but inconsistent, and are directly related to the type of stimulus presented, such as turning head towards sound or focusing on presented object. May follow simple commands in a consistent an d delayed manner.
IV. Confused-agitated. Patient is in a heightened state of activity and severely confused, disoriented and unaware of present events. Behaviour frequently bizarre and inappropriate to his immediate environment. Unable to perform self-care. If not physically disabled, may perform automatic motor activities such as sitting, reaching and walking as part of agitated state, but not necessarily as a purposeful act.
V. Confused-inappropriate. Non-agitated. Patient appears alert and responds to simple commands. More complex commands produce responses that are non purposeful and random. Patient may show some agitated behaviour but it is in response to external stimuli rather than internal confusion. Patient is highly distractible and generally has difficulty in learning new information. Manage self-care activities with assistance. Memory impaired and verbalisation often inappropriate.
VI. Confused appropriate. Patient shows goal-directed behaviour but relies on cuing for direction. Can relearn old skills such as activities for daily living but memory problems interfere with new learning. Beginning awareness of self and others.
VII. Automatic-appropriate. Goes through daily routine automatically but robot-like with appropriate behaviour and minimal confusion. Shallow recall of activities superficial awareness of, but lack of insight to. condition. Requires at least minimal supervision because judgment, problem solving, and planning skills are impaired.
VIII. Purposeful-appropriate. Alert and oriented. Able to recall and integrate past and recent events. Learn new activities and continue home living skills. Deficits may, however, persist in stress tolerance, judgment, abstract reasoning, social, emotional and intellectual capacities.
Glasgow Coma Scale
Standardised system used to assess the degree of brain impairment and to identify seriousness of injury in relation to outcome. Involves three determinants - eye opening, verbal response and motor response (movement). Evaluated separately according to numerical value that indicates level of consciousness and the degree of dysfunction. Scores run from a high 15 to a low 3. Considered to have experienced "mild" brain injury if score is 13 to 15 Range 9 to 12 considered "moderate" and 8 or less "severe" brain injury. Terms "mild, moderate and severe" used as relative terms to describe severity of injury and do not trivialise the seriousness of any brain injury.
In an emergency room setting arrival of comatose patient triggers process in which history-taking, diagnosis and treatment are carried out simultaneously as required for optimal management. Neurological examination is portion of this process, and in itself can be accomplished in no more than a minute of two. IV glucose may be life-saving for hypoglycemic condition (low blood glucose) and will do little to worsen patients with hyperglycemic (too much blood glucose).
Clinical evaluation is critical (CT/MRI scans often uninformative during the early course of comatose patient. Motor response to pain - patient direct one or more limbs toward stimulus in attempt to ward it off. Movement resembles normal response although it may not be as swift of accurate. Decorticate posturing - upper extremities flexed at elbows and wrists, forearms pronated and shoulders adjusted. Lower extremities extended. Decorticate posturing occurs in diencephalic or high mid-brain lesions. Indicates higher level of function than decerebrate posturing. Decerebrate posturing - shoulders adjusted and internally rotated, elbows extended and forearms pronated. Lower extremities extended. Decerebrate posturing seen in lesions of brain stem tegmentum below the red nuclei (midcollicular line) and above vestibular nuclei (lateral vestibular nucleus provides extensor tone via the lateral vestibulospinal tract).
Coma - State of Profound Unconsciousness
Proprioceptive and other sensory messages sent to brain into brain stem and other areas below cortex (thinking part), the brain did not have to be awake to benefit from stimulation. Little or no stimulation through five senses - vision, hearing, touch, taste and smell. Odd situation - excited and encouraged by any sounds but then the world wants people like that to be quietened, even given sedatives! Comatose patient probably placed in the decerebrate position and if eyes open first only direction is to see up. Probably a very non-stimulating ceiling. Or the floor if placed in a "strykker frame" to prevent bed sores. It may appear that there is little in the way of stimulation but that is not quite true. The attention by way of monitoring, respirators, IV feeding tubes placed everywhere. Nevertheless physical stimulation is limited and is probably not enough to bring a patient around from a comatose state. Not all comatose patients respond in the same way to stimulation to the point of recovery.