Chapter 4 – Acquired Disorders
Traumatic Brain Injury/Head Injury
Peak years for TBI are in the 15-24 year range. 65+ and younger than 5 are the next
Males are more likely to sustain TBI than females (except in the 65+ and 5 and under
The severity of a TBI is measured by:
1. Length of posttraumatic amnesia (PTA)
2. Depth of unconsciousness, usually measured after resuscitation. Measured with
Glasgow Coma Scale (GCS), 3 being the worst and 15 being the best
3. The length of unconsciousness and/or presence of neurological signs
Open Head Injury
Def.: occurs when an object penetrates the skull and exposes the brain to the elements
Rate of death is higher with an open head injuries. Mortality risk is related to the type of
object impinging on the brain.
• An object that ricochets or causes debris to be driven further into the brain will
cause more damage
• A clean wound implies that the damage is mainly along the path of the invading
• Secondary effects may include hypotension (low blood pressure), hypovolemia
(low blood volume), contusions, and intracranial hematomas
Neuropsychological difficulties are usually linked to the site of the lesion. Patients also
tend to show the effects of general diffuse brain impairment – difficulties with
concentration, attention, memory, and overall mental slowing.
Time is a crucial factor – sooner the treatment is begun, the greater the chance of
survival. Open head injury is highly related to epilepsy, 80% if patients experience
seizures in the first 24 hours.
Closed Head Injury
Def.: impact from an accident or injury causes brain damage but does not penetrate the
skull. Occurs in two stages:
• Coup: initial impact as an object or event impinges on the skull covering the brain
• Countercoup: secondary impact as the brain ricochets back and forth or side to
side within the skull Several difficulties involved:
• The force in which the coup is applied to the brain is critical
• The force during the countercoup when the brain jostles back and forth
• More force is more dangerous. Primary difficulties:
o Diffuse white matter damage: diffuse axonal injury is caused by the
acceleration and deceleration of the brain impacting against the skull
o Contusion (bruising): often occur under the frontal and temporal poles
where the shearing forces of the brain are impacting on the sharpest and
most confined parts of the skull. Can occur under the point of impact or at
o Hemorrhage: occurs when blood vessels supplying oxygen to the brain
• Secondary damages:
o Hematomas, cerebral hemorrhage, infection, hydrocephalus, and anoxic
damage caused by breathing difficulties or low blood pressure
o Neurochemical difficulties such as excitotoxicity, cell membrane
degradation, cellular edema, and changes in cellular events
Neuropsychological difficulties for individuals with closed head injury are similar to those
with open head injury except they may be less severe. Typical symptoms include:
• Impaired speed of information processing, difficulties with concentration and
attention, memory deficits, and problems with reaction time
Often experience behavioural and/or personality changes subsequent to the injuries.
Most will experience some form of depression or other emotional difficulty usually
because of changes in life circumstances.
• PTSD can occur if the injury was caused by a trauma.
• Very often patients describe an inability to deal with strong emotions
• Can look normal but cannot function as before, cause many difficulties with
relationships and employment
• Often a lack of awareness of their behavioural, cognitive, or physical deficits
Treatment for closed head injury is similar to open head. Very important is need to
control brain swelling.
Postconcussion Syndrome Def.: constellation of physical and psychological symptoms that may occur as a result of
medically verifiable concussion.
Concussion is mainly caused by diffuse axonal injury. Symptoms include loss of
consciousness, PTA, and sometimes seizures. Considered low on the spectrum of TBI,
compared to open or closed head injuries.
Only substance in the toxic grouping that has positive protective effects and negative
• Protective: alcohol, especially wine, has protective effects from cardiovascular
and cerebrovascular disease (in moderation)
• Negative: when not used in moderation, may cause moderate to severe
difficulties for the central nervous system.
Alcohol abuse: excess use of alcohol for a period of 12 months. During this time, the
use of alcohol has been shown to have a negative impact on the individual’s social or
Alcohol dependence: same as alcohol abuse, with the inclusion of tolerance and/or
• Tolerance: need for more and more of a substance to achieve the same level of
intoxication or ‘high’
• Withdrawal: pattern of symptoms that occur after the cessation of substance
o May include nausea, headache, shakiness, and desire/craving for the
Binge drinking: drinking of an excessive amount of alcohol within a short period of time
often with the intent of becoming quickly intoxicated
• Binge drinkers appear to be less prone to alcohol related cognitive deficits than
those with a heavy daily intake
Alcohol is a central nervous system depressant – slows/depresses the functioning of
structures within the central nervous system. Has the paradoxical effect – produces a
feeling of euphoria before the onset of depressive feelings.
Alcohol is a neurotoxin: substance considered to be a poison within the central nervous
system. It’s metabolised differently than other drugs, in a process called zero-order
kinetics: metabolism at a steady state regardless of quantity of substance consumed
Females metabolize alcohol slower than males Chronic alcohol use may cause cognitive deficits including difficulties with complex
visuospatial abilities and psychomotor speed.
• Well learned tasks such as arithmetic, language, and attention are not as greatly
• Memory can be affected but not evident in all users. As memory task increases in
complexity, there is a more of a chance for impairment
Alcohol dementia: dementia due to alcohol consumption
• Sometimes difficult to distinguish from other dementias – can be identified by
past alcohol use
• Person can recover some abilities with abstinence
Korsakoff’s syndrome: memory and cognitive difficulties due to alcohol consumption and
the absence of the vitamin thiamine
• May appear to have manic confusion and be unable to clearly state thoughts
• Exhibits disoriented eye and limb movements
• Can be treated if thiamine is given as soon as possible
• 1-2 weeks: may show myriad of cognitive and memory deficits
• After this, the beginning of abstinence occurs in which the greatest amount of
return of functioning is evident
• Next 3-6 weeks, return of function slows down
Street Drugs (Illegal Substances)
Many drugs are ploydrug users so it’s hard to distinguish what drug is having what
Has psychoactive and physiological effects which vary based on whether the substance
is smoked, sniffed, or ingested.
Effects have been described as pleasant and/or unpleasant often related to variables
such as mental state of the user at the time of use and the expectations of the user in
terms of the effects of the drug.
Has the potential to induce hallucinatory experiences and emotional states as well as
time distortions and memory loss. The intensity is doss dependent
• High doses may result in psychotic-like symptoms • Lesser doses may result in psychotic may result in psychotic symptoms in those
individuals who have a predisposition or vulnerability to schizophrenia
Those who initiate use at a younger age (less than 17) are more likely to develop
neuropsychological deficits than those who begin at a later age.
Some studies show personality changes with heavy usage. Most common symptoms
include emotional blunting, mental sluggishness, apathy, restlessness, mental
confusion, and an amotivational syndrome.
Considered a central nervous system stimulant. It’s highly addictive due to the ‘rush’,
which is expressed through inhalation. Much less of an effect when it is taken
• Other effects: increased alertness and arousal and an increased sense of well-
being/confidence. These appear positive and will lead to continued drug use.
Cocaine increases the level of dopamine in the reward circuits in the brain, leading to
craving and a higher threshold for a euphoric reaction to the drug.
• Originally can work as aphrodisiac but will eventually lower libido
• Other reactions include paranoia, delusions, hallucinations, and panic attacks
In the beginning it acts as a pleasure inducer but with repeated use, it damages the
brain’s pleasure centers.
Long-term users may have many cognitive deficits with memory and concentration
difficulties being the most significant. Seizures can occur with new and habitual users.
Hypertension and other central nervous system issues may occur. Show issues with
Withdrawal is neither life threatening or too painful.
• Symptoms like restlessness, confusion, abnormal muscle movements have
• There may not be a complete rate of return of functioning
First opiate drugs were derived from the opium poppy – heroin, morphine, codeine.
They were originally viewed as a form of cure-all.
In 1914, the Harrison Narcotics Act was passed. Narcotics were now prescription-based
1973, discovered that there were specific opiate receptors in the brain. After this came
the discovery that the brain produced its own chemicals termed enkephalins and endorphins (brain hormones which help alleviate pain or lead to a feeling of euphoria),
that fit into these receptors. These are released during stress or pain.
• Opiates compete with endorphins for the receptor sites.
Major medicinal use for narcotics is pain control.
Tolerance develops for all of the narcotics and is often a problem for individuals who use
the drugs appropriately for pain control. Cross-tolerance also develops – if tolerant to
one drug, they will be tolera