Brain Lesions, 
           Medications and it's Side Effects
                            
                            
                    by  Adel Olvera
                            
                    Neuropsychology
                            
                            
                 Traumatic Brain Injury
                            
     Traumatic Brain Injury, TBI, can be fatal if the
injury is ignored and treatment is evaded.  Some examples
of the different types of brain injuries are skull
fracture with and without concussion, contusion,
hemorrhage, laceration to the brain and many different
types of intracranial injury resulting from blows to the
head.  Medications vary depending on the localization of
the injury and the symptoms that occur after TBI. 
Unfortunately, there are times when nothing can be done
to improve the injury or it's symptoms.  Medications
prescribed after TBI can cause physical and behavioral
side-effects. 
     According to Silver, Yudofsky, and Hales (1994), the
larger majority of patients with brain injury are those
that are suffering with mild brain injury.  A prognostic
indicator classifies patients with either trivial, mild,
moderate or severe brain injury.  A score of 13-15 on the
GCS, Glasgow Coma Scale, classifies patients as having
mild brain injury (Silver, et al, 1994).  Indicators of
mild brain injury are:  feeling stunned or dazed, drowsy
or indifferent, disoriented or having trouble with
complex commands, and complaints of headache, nausea or
vomit (Silver, et al, 1994).  Patients with moderate
brain injury will experience "more than a 30-minute
period of unconsciousness or posttraumatic amnesia and/or
had a skull fracture" (Neuropsychiatry of T.B.I., 1994,
p. 515).  Severe brain injury includes "evidence of brain
contusion, hematoma, or 24 hours of unconsciousness"
(Neuropsychiatry of T.B.I., 1994, p. 515).  Doctors will
gear towards medications as a next step to help eliminate
symptoms that patients experience after TBI.  
     Correct usage of neurological drugs can be effective
for a patient, but there are risks that need to be taken
into account.  Side-effects can occur if the medication
taken incorrectly, or prescribed inaccurately.  Opposing
reactions can manifest themselves emotionally or
physically.  One can experience, hallucinations,
aggression, nightmares, weakness, fatigue and/or nerve
damage in the central nervous system.  For instance,
medication given to patient who have symptoms of seizures
due to a discernible local lesion in the brain may be
prescribed carbamazepine.  Carbamazepine (a.k.a.: 
tegretol) can cause drowsiness, dizziness, skin rashes
(Cutting, 1967) and aggression (Silver et al., 1994). 
     Depression is a behavioral change in TBI patients. 
It is believed that depression is a result of irrational
thinking.  A patient's depression can occur because of
premorbid social factors, and/or because they tend to
isolate themselves.  They either feel weak, too sick to
go out, have suicidal tendencies,  feelings of
worthlessness, and/or have no hope in recovery.  Research
conducted by Robinson, Starr and Kubos indicate that
depression is more occurring in patients with left
dorsalateral frontal cortex and left basal ganglia
lesions; due to the of damage to the left hemisphere,
disruption of it's ascending noradrenegic or serotnergic
pathways and their related behavioral functions (Silver
et al., 1994). 
     Lipsey, Robertson and Peterson (Silver et al., 1994)
state that tricyclic antidepressants have anticholinergic
effects that may interfere with cognitive and memory
functions yet can lower seizure threshold.  Tricyclic
drugs "operate by preventing the presynaptic neuron from
reasbsorbing catechloamines or serotonin after releasing
them; thus, the neurotransmitter remains longer in the
synaptic cleft and continue stimulating the postsynaptic
cell" (Biological Psychology, 1995, p. 555).  Likewise,
the lack of norepinephrine, serotonin and dopamine is a
known cause of memory failure (Kalat, 1995). Kruk and
Pycock (1979, p. 59-61) states that MAO inhibitors, which
are known to work against depression, increase the levels
of noradrenaline in the brain, and inhibits the reuptake
of serotonin.  Safer drugs, with less side effect can be
used, such as, fluoxetine. It's side effects are those of
"headaches, gastrointestinal complaints and insomia"
(Neuropsychiatry of T.B.I., 1994, p. 238).  
     L-dopa is a medication well known for it's
treatments to prevent Parkinson's disease, attention
deficits, agitation, and other forms of impulse
dyscontrol (Silver et al., 1994).  A variety of symptoms
reveal the existence of side effects.  Behavioral
changes, such as depression, are at greater risk with
prolonged use of L-dopa.  Mania, hallucinations, and
aggression are symptoms that are most frequent in elderly
patients.  Symptoms of nightmares occur for patients
whose dosage have been increased (Silver et al., 1994). 
Additionally, sleeping disorders, nausea, low blood
pressure, and stereotyped movements are other symptoms
that come with L-dopa; with the possibility to worsen if
taken for a prolonged period. (Kalat, 1995).  
     Parkinson's is a neurological disorder caused by
result of cerebral injury or disease (Kruk et al., 1979). 
Damage to and the loss of dopamine neurons in the basal
ganglia (Shader, Dimascio, 1970), pars compacta of the
substantia nigra up to the dorsal striatum result in
Parkinson's disease (Silver et al., 1994).  "Dopamine
itself is an organic base which bears a positive charge
at neutral pH and thus cannot pass the blood
barrier...dopa, the biosynthetic precursor of dopamine, 
bears no net charge and can enter neural tissue from the
bloodstream" (Psychotropic Drug Side Effect, 1970, p.
99).  Dopamiergic nerve terminals take L-dopa, as well as
some neuronal tissues (e.g. glial cells) to the brain. 
Some of all L-dopa is then decarboxylazed to dopamine,
diffused into the synaptic cleft and imitates dopamine
receptors.  
     Certain patients develop high tolerance for L-dopa,
leading to an increase in medication dosage.  Side
effects increase when the L-dopa remaining decarboxylase
outside the central nervous system.  Patients will either
add another drug to their diet (e.g. a decarboxylaze
inhibitor) that reduces side effects, reduce their
initial dosage of L-dopa or completely remove intake of
L-dopa.
     Antipsychotic or neuroleptic medications given to
patients after TBI can also cause serious side effects. 
Neuroleptic drugs have been classied into three different
types, each with variant strengths: low, medium, and
high.  Thioridazine, mesoridazine, and chlorpromazine,
(are of medium potency) "are sedating, have greater
anticholinergic properties, and cause greater orthostatic
hypotension" (Silver et al., 1994, p. 649). 
Antipsychotic drugs block postsynaptic dopamine receptors
and cause different extrapyramidal side effects (e.g.,
parkinsonian:  drooling, rigidity, tremors; acute
dystonic syndrome: distortions of facial musculature or
back, spasms; akinesia:  difficulty in initiation, speech
and movement; etc.)(Silver, et al., 1994).  Neruroleptic
medications are given to patients with Psychosis after
TBI, because it can reduce hallucinations, delusions and
other symptoms of schizophrenia (Kalat, 1995). 
Antipsychotic drugs don't actually cure Psychosis rather
control it (Kalat, 1995) making it a never ending
process.   
     Some patients are told that side effects will cease
when treatments are complete, and in some case patients
are not being lied to.  Though, personal research is
recommended and can be useful in preventing unnecessary
symptoms due to the intake of harmful medications.  For
example, Bromocriptine is a drug given to TBI patients
with symptoms of Parkinson's disease, mania, paranoia,
aggression, cognitive dysfunction and arousal after TBI. 
According to Silver, Yudofsky, and Hales (1994) mania may
persist after the drug is withdrawn.
     Physical and behavioral side-effects can occur due
to a lack of knowledge in drug chemistry and its
interactions with human chemistry.  After TBI there 
are neurotransmitter changes of norepinephrine,
serotonin, dopamine, and acetylcholine that occur in the
body.   There is a increase of plasma norepinephrine
after acute head injury, and was compared with more
severe injury and poorer clinical outcome.  The 5-
Hydroxylindoleacetic acid was below "normal in conscious
patients while normal in patients who were unconscious"
(Silver et al., 1994, p. 637).  The decline of serotonin
and norepinephrine occurs are due to the damage in the
nerve tracts of these pathways (Silver et al,. 1994). 
     It is important that people understand the functions
of human biology and take the take to read general
guidelines in pharmacological treatment.  Silver,
Yudofsky and Hales recommend:
          "1.  Start low; go slow.
           2.  Therapeutic trial of all medications.
           3.  Continuous reassessment of clinical
                    condition.
           4.  Monitor drug-drug interactions.
           5.  Augment partial response" (1994). 
Make sure that the physician is following these
guidelines and never hesitate to ask the physician any
questions.  Taking precautions steps can save the stress
accumulated from side effects. It can affect the life
structure of the injured patient and the lives of family
members. 


References Cited:

Cutting, W. C.  (1967).  Handbook of Pharmacology.  New
     York, NY:  Apppleton-Century-Crofts.  
Kalat, J. W. (Eds.). (1995).  Biological Psychology.
   Pacific Grove, CA:  Brooks/Cole Publishing   Company.
Kruk, Z., & Pycock, C.  Neurotransmitter and Drugs.
    Baltimore:  University Park Press.
Silver, J., Yudofsky, S., & Hales, R. (1994).
     Neuropsychiatry of traumatic brain injury.
     Washington,
D.C.:  American Psychiatric Press,      Inc.  
Shader, R. I., & DiMascio, A. (1970).  Psychotropic
     Drug Side Effects.  Baltimore, MD:  Waverly Press,
     Inc.

Copyright © 1997, Dr. John M. Morgan, All rights reserved - This page last edited March 17, 1997
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