MEDICATION PRESCRIPTION:
Unless specifically indicated, medications are
generally not necessary in a CHIT. However, even
if they may not be necessary at one point, these
ideas may serve as a guide for future management
of individual patients. Treatment is commonly
based on symptom alleviation although chemical
regulation with buspirone or putting out fires
with anticonvulsants is sometimes based on treating
the underlying cause.
The four major groups of treatment
(neuromodulation, anticonvulsants, sleep disruption,
antidepressants) and the specific conditions linked
with these medications
1. NEUROMODULATION OPTIONS
Post traumatic head injury characterologic changes
and Personality Disorders and Anxiety Disorders
Following transient traumatic head injury, a range
of central nervous system dysfunctions may ultimately
influence the behavior we site as characterological
disturbances. Organic links (from diverse etiologies)
have been noted particularly in antisocial personality
by Lewis and Bella (1976), Robins (1966), Thomas
and Chess (1977l, and Tucker and Pincus (1980).
Usually these correlate with antisocial behavior
and delinquency that relates to EEG abnormalities,
delayed reaction times, and seizure disorders.
(Tucker, Neppe 1988) The heterogeneous and poorly
validated condition of borderline personality
disorder with fluctuations in affect, intensity
of experience, irritability, frequent suicidal
behaviors, aberrant behavior spells, and brief
psychotic features with total recovery all suggest
some temporolimbic instability. (Tucker, Neppe
1988, 1994); (Tucker et al 1986)
Anxiety is a ubiquitous psychiatric
symptom. Episodes of anxiety, particularly so-called
"panic attacks" may correlate in our
experience with complex partial seizures. Such
events were recognized by Hughlings Jackson last
century. (Neppe, 1984A) Most anxieties with head
injuries are likely to be on the psychological
side not due to brain injury however.
BUSPIRONE (BUSPAR) medication. This
is a prime drug for the patient with a CHIT because
of its versatility and safety. The buspirone can
be used for the approved usage of relieving anxiety
/ mixed anxiety depression in the post-traumatic
CHIT. In this instance, the post-synaptic serotonin
1A partial agonist effect comes into play. The
usual dose for anxiety is 10 mg t.i.d., for mixed-anxiety
depression is 15 mg t.i.d. (Neppe, 1990 A, 1989A,
1993A) However, it should alleviate the following
symptoms
sometimes linked with anxiety which are frequently
relate to post-concussional phenomena of the CHIT:
concentration disturbance and also the spectrum
of agitation, irritability, frustration, anger,
aggression (where no FDA approved drugs exist):
Two dose levels of dosage are useful - low e.g.
5 mg t.i.d. which probably reflects autoreceptor
raphe serotonergic nuclei effects; and high for
considerable agitation and co-existing other symptoms
e.g. 20 mg t.i.d. probably reflecting a predominantly
serotonin 1A weak agonist effect. The low dose
is based on the uncontrolled work of Neppe on
non-organic patients and Ratey on mental retardates,
the higher dose on Neppe's research. In many patients,
we suggest initiating dosage at 5 mg t.i.d. built
up gradually by increasing by 5 mg every 3 days
to a initial aim level of 60 mg per day: if the
patient develops non-vertiginous dizziness then
drop the dose by 5 mg per day and continue the
taper of dose until no dizziness occurs. Additionally,
many CHIT patients reveal a predisposition towards
obsessionality . Doses of e.g. 20mg t.i.d. probably
reflect a predominantly serotonin 1A weak agonist
effect and could be useful here - the only approved
drugs for obsessive compulsive disorder - Clomipramine
(Anafranil) and SSRI drugs like fluoxetine (Prozac)
often have significant side-effects in this population.
Important relevant side-effects are:
- nonvertiginous dizziness - if this occurs
the patient could cut down the dose by 5 mg
per day, the patient should contact the treating
physician and continue the dose at this lower
level without continuing to build up the dose
at that time.
- nausea - this suggests that the medication
should be taken with mealtimes - breakfast,
lunch and dinner.
- headache and restlessness.
- the occasional paradoxic accentuation of
anger or confusion in the organic CHIT patient
- usually an indication that anticonvulsant
is necessary.
2. ANTICONVULSANT OPTIONS
Seizure
Disorders
A person is only epileptic when he has seizures
recurrently. An epileptic seizure involves paroxysmal
cerebral neuronal firing which may or may not
produce disturbed consciousness and / or other
perceptual or motor alterations (Neppe, 1988A,
B). The most classical and common epileptic seizures
are of the "grand mal" or generalized
"tonic - clonic" kind. These usually
involve relatively short (10-30 seconds) tonic
movements with marked extension / flexion of muscles
but no shaking and then a longer (15-60 sec) clonic
tonic manifesting as rhythmic muscle group shaking.
These movements may be associated with a phase
of laryngeal stridor due to tonic muscles manifesting
as a high pitched scream sound. Urinary and occasionally
fecal incontinence may occur due to sphincteric
change and the seizures are almost invariably
followed by headache, sleepiness and / or confusion.
When preceded by perceptual, autonomic, affective
or cognitive alterations such seizures are secondarily
generalized, as opposed to no original locus of
firing producing focal features prior to the tonic
clonic movements (generalized from the start)
(Neppe, 1982 A ). The different epileptic seizures
are classified in Table 1.
Seizures or other paroxysmal neurobehavioral
disturbances which may not qualify as seizures
because the actual phenomena are not proven to
be seizures are not insignificant post-traumatically.
Until all variants are measured it would be difficult
to estimate exact incidence. This is particularly
so in the context of transient closed head injury.
(CHIT) There is a dichotomy of the possibly 90%
of epileptics who constitute the epilepsy standard
patient who have no more psychopathology than
the average patient and the epilepsy plus patient
- a minority of epilepsy patients having behavioral
or psychiatric abnormalities (Neppe, Tucker 1992).
Seizure disorders present with a high incidence
of behavioral disturbance, which may initially
be interpreted as psychiatric in origin (Neppe,
Tucker, 1989, 1994). Many of these relate to the
temporal lobe of the brain. The features of temporal
lobe epilepsy are so varied and so protean that
it is necessary to classify them. Neppe has suggested
the term "possible temporal lobe symptoms"
(PTLSs) for this (Neppe, 1983 A). These are features
which can be induced by stimulating areas of the
temporal lobe during neurosurgery. These symptoms
only become specific symptoms of temporal lobe
dysfunction if their occurrence is validated empirically
during a seizure - either through observation
or by the electroencephalogram (hence the word
"possible" in possible temporal lobe
seizures) ( Table 2 ) (Neppe, 1983 B). Using a
phenomenological analysis, Neppe was able to demonstrate
that the symptom of deja vu commonly regarded
as symptomatic of temporal lobe epilepsy indeed
had a very special phenomenologic quality in patients
with temporal lobe epilepsy (Neppe, 1983 A, 1983C
). This involves its association with post-ictal
features such as sleepiness, headache and clouded
consciousness and its link in time with these
features. This association provides an excellent
clue to the existence of temporal lobe epilepsy.
Deja vu is a normal phenomenon occurring in 70
percent of the population and unless such phenomenological
detail is obtained, patients' symptomatology may
be misinterpreted. Neppe has similarly done such
a study with olfactory hallucinations (Neppe,
1983 B, D, 1982 B). A specific type of temporal
lobe epilepsy olfactory hallucination could not
be demonstrated although there were suggestive
features (Neppe, 1984B). A major message, therefore,
may be the relevance of adequately assessing the
symptomatology of patients presenting with epilepsy.
It may be that this is a direction as relevant
as electroencephalographic monitoring (Neppe,
1993 B).
Theoretical biases: Kindling
and Chindling
Kindling may be relevant in head injury. Generally
several events would be required to trigger such
a phenomenon but CHIT theoretically may the straw
that broke the camel's back. We discuss kindling
briefly below.
Kindling involves the progression
of increasingly severe seizure manifestations
in response to electrical stimuli of various areas
of the brain such as the hippocampus, amygdala,
pyriform cortex, or basal ganglia. Such stimulation
is initially sub-threshold, but becomes threshold
when administered repetitively. These sub-threshold
changes, which have been demonstrated in numerous
animal species, at times manifest with behavioral
changes sometimes preceding the motor seizures
(Neppe, 1985A,B,C). Neppe recognized that there
are distinct biochemical and other differences
between so-called electrical kindling and the
chemical induction of the process and so developed
the term chindling for the chemical induction
of increasingly severe seizure manifestations
in response to general chemical stimuli (Neppe,
1989 B).
Kindling is increasingly difficult
to induce with the added degrees of encephalization
in primates. If, indeed, the kindling phenomenon
occurs in man, it would probably take many years.
There is indirect evidence for its occurrence
in the development of mirror foci, generalization
of seizures, the alcohol withdrawal paradigm,
and possibly paradigms of response pertaining
to nonresponsive psychosis (Tucker, Neppe, 1988,
1991). However, kindling has become a very useful
theoretical concept to rationalize interventions
pertaining to adjunctive drugs, particularly anticonvulsants.
Whether or not kindling is shown to be an artifact
or not is probably not of vital importance, for
its role may be as a stimulant to further research.
ANTICONVULSANT PRESCRIPTION
The preferential anticonvulsants in this instance
are not necessarily for a seizure indication,
per se. The subpopulation of CHIT being treated
is the focal residual group. They may manifest
with frank post-traumatic seizures, however, they
may have atypical spells manifesting as the various
kinds of episodic events that we have called paroxysmal
neurobehavioral disorder (PND). Diagnosis is based
clinically, on EEG and on anticonvulsant responsiveness.
The management of epileptics presenting
with behavior disturbance is closely linked to
the discussion of epilepsy in relation to psychopathology.
The heterogeneity of such conditions implies a
heterogeneity of management which is patient based
and individually tailored (Neppe, 1988).
The most important single principle
is anticonvulsant monotherapy. It has been well
demonstrated that the degree of seizure control
is not increased by increasing the number of anticonvulsant
medications. (Neppe, Tucker 1988 A, B) It is more
important to achieve adequate anticonvulsant dosage
and therapeutic ranges on blood levels are often
helpful indicators. However, the object should
be to adequately control all the patient's seizures
and the choice of anticonvulsant is equally important.
Management of patients with seizure disorders
involves primarily appropriate use of anticonvulsants
(Neppe, Tucker, 1988B). In addition, counseling
and the various aspects of psychosocial support,
allowing the patient to live as normal a life
as possible, and to be supported within the framework
of the environment, is also important.
a. CARBAMAZEPINE (Tegretol) is the
primary drug in this group for the CHIT indication
as it seems to have a specific psychotropic effect.
We use it predominantly in the context of temporal
lobe phenomena. It should not to be generically
substituted (Neppe et al, 1988C ). The carbamazepine
in this instance can be used for the approved
usage of relieving seizure disorders or any incidental
neuralgia and sometimes fibromyalgia (unapproved
and unproven). In seizures, the anticonvulsant
effect comes into play. The usual dose for seizures
are 200-400 mg t.i.d. or q.i.d. based on monitoring
serum levels to 8-12 ug/ 100 ml and clinical responsiveness
and we have found usually slightly lower doses
to be adequate in atypical spells, PND and temporal
lobe dysfunction e.g. 200 mg tid.
Carbamazepine should alleviate the
following symptoms which are not FDA approved
(and no FDA approved drugs exist): agitation,
irritability, frustration, anger, aggression,
mood lability, temporal lobe symptomatology: The
dose levels are probably in the low therapeutic
anticonvulsant range e.g. 6-9 ug/ 100 ml and frequently
correspond with an initial target dose of 200
mg t.i.d. The low dose is based on the double
blind controlled work of Neppe on patients with
EEG temporal lobe abnormalities and refractory
psychosis with hostility and a follow-up retrospective
chart review on hostile atypical psychotics (Neppe
and Bowman, 1991) in which the EEG was normal.
The mechanism may be via kindling or chindling
and episodic phenomena respond best (Neppe, 1990
B).
Generally, a starting dose of 100
mg bid build up by 100 mg every three days to
an initial target dose of 200 mg t.i.d. Important
side-effects relevant for the patient include:
- Signs of neurotoxicity : Dizziness, sedation,
diplopia and nausea. Each of these symptoms
may reflect toxicity so that consideration
can be given to one dose being held and the
dose dropped by 100 mg per day pending a blood
level if necessary.
- Allergy: Usually a rash - possibly in as
many as one in eight patients - occurs; far
less commonly and more seriously a sore throat,
fever or mouth ulceration may happen: The
patient should stop the medication pending
discussion with the treating physician to
establish if the reaction is drug related.
- Extremely rare is the occurrence of bone-marrow
depression which is an idiosyncratic reaction.
There appears to be no correlation of the
frequent and expected drop in white cell count
with this or other immunologic infection predisposition.
- Tegretol induces enzymes and may impair
control of conception by oral contraceptives.
The usual practice has been to increase the
OC dose slightly if not contra-indicated for
any reason but safer is to add a second contraceptive
method as well.
Prior to beginning the carbamazepine
treatment, the following baseline blood tests
should be performed: Complete blood count including
differential cell count with optional platelet
and reticulocyte count. Hepatic enzymes including
Gamma Glutamyl Transferase. Electrolytes. At subsequent
visits, the carbamazepine levels can be measured
and after establishing a new baseline the CBC
and GGT can be monitored as necessary. Folate,
a B vitamin, supplementation is often necessary
based on possible subclinical deficiency induced
by carbamazepine which induces hepatic enzymes
- folate is a co-enzyme in this cycle. Doses of
5 mg daily are recommended. Calcium supplementation
e.g. as gluconate is also relevant sometimes.
One mechanism may be carbamazepine enzyme induction
producing subclinical Vitamin D deficiency particularly
in a cloudy climate.
b. Other anticonvulsant options
are briefly outlined below:
b. 1. PHENYTOIN (DILANTIN) Adequate
control of seizures with only occasional episodes
suggesting maintaining this drug. However, high
therapeutic levels e.g. 20 ug/ ml are associated
with significantly more cognitive side-effects
than lower levels. Rigidity, slowed thinking,
irritability, sedation, poor psychomotor control
and responsiveness are examples. Consequently,
lower doses may be more logical even with adjunctive
second anticonvulsant, if necessary. Folate and
Vitamin D and Calcium supplementation should be
considered. The initial aim dosage is 300 mg daily
, as a TID or QD dosing. Phenytoin can be given
intravenously if necessary. Important side-effects
relevant for the patient include:
- The change to zero order pharmacokinetics
with potential toxicity with slight dose alterations
or other drugs added.
- The gum hyperplasia is a somewhat disabling
long-term effect that is extremely common.
- Allergic reactions include rash commonly,
neurotoxicity frequently and very rarely bone-marrow
phenomena.
- Potent enzyme induction with raised hepatic
enzymes produces common drug interactions.
b.2. DIVALPROEX SODIUM (DEPAKOTE).
Initiation of DIVALPROEX SODIUM (also called Valproate)
(DEPAKOTE - not a generic) may be useful particularly
with residual focal frontal lobe phenomena. The
Valproate has an approved usage of relieving seizure
disorders and for prophylaxis of bipolar illness
and for headache prophylaxis. However, it could
alleviate the following symptoms which are not
FDA approved: agitation, irritability, frustration,
anger, aggression, mood lability, temporal lobe
symptomatology (no FDA approved drugs exist) but
there is limited clinical use in these areas because
frequently there is limited effectiveness. A starting
dose of 250 mg t.i.d. is suggested. The usual
dose for seizures are 250-1000 mg t.i.d. or q.i.d.
based on clinical responsiveness mainly but also
-far less reliable with valproate - monitoring
of serum levels to 70-100 ug/ 100 ml. For non-approved
uses slightly lower doses e.g. 250 mg-500 mg t.i.d.
or q.i.d. with similar blood levels to seizures
may be appropriate. Whether the mechanism then
is anticonvulsant or psychotropic is unknown.
A major advantage of valproate is
it is generally well tolerated with few side-effects
and less sedative than carbamazepine. Important
side-effects relevant for the patient include:
- Nausea is common: give with meals.
- Dizziness, sedation and diplopia but these
are uncommon. Each of these symptoms may reflect
toxicity so that consideration can be given
to one dose being held and the dose dropped
by 250 mg per day pending a blood level if
necessary. Supplemental carnitine has been
suggested both to prevent hepatotoxicity and
diminish any cognitive side-effects. Dosing
is disputed but 500 mg qd may be reasonable.
- Allergy is rare.
- Extremely rare is the occurrence of hepatotoxicity.
There appears to be a correlation with anticonvulsant
polytherapy in infants and in adults the drug
should be safe.
- Most psychotropics will push up the Valproate
level and it will do likewise. Carbamazepine
may lower it. Valproate does not induce enzymes.
- Many patients complain of weight gain which
may be the most significant common side-effect
and reason for discontinuation.
Prior to beginning the Valproate
treatment, the following baseline blood tests
should be performed:
- Complete blood count including differential
cell count with optional platelet and reticulocyte
count.
- Hepatic enzymes including Gamma Glutamyl
Transferase, Bilirubin, Prothrombin.
- Electrolytes.
- At subsequent visits, the valproate levels
can be measured and after establishing a new
baseline the CBC and GGT can be monitored
as necessary.
b. 3. GABAPENTIN (NEURONTIN) This
new anticonvulsant has the advantage of low toxicity,
low range of side-effects and no known drug interactions.
Serum levels are not helpful for clinical practice
as they are non-correlative with therapeutic range
or toxicity and they are, in general, unavailable.
Technically gabapentin is an adjunctive anticonvulsant,
but it may be tried in monotherapy for specific
symptoms. Doses of 100 mg t.i.d. are low average
although 20% get sedated so start low 100 mg daily
building by 100 mg QOD till better control e.g.
300 mg t.i.d.
b.4. LAMOTRIGINE (LAMICTAL) This
new anticonvulsant in the United States had been
marketed in numerous countries before that. It
has remarkable effects on some although in our
experience patients may initially become paradoxically
worse with each increase in dose. Like gabapentin,
serum levels are unnecessary and unavailable.
Technically, it too is an adjunctive anticonvulsant,
but it may be tried in monotherapy for specific
symptoms. Doses of 25 mg daily built up to 100-200
mg bid over several weeks are average.
b.5. TOPIRAMATE (TOPIMAX) and TIAGABINE
(GABATRIL) These are new anticonvulsants in the
United States Tiagabine marketed October 1997).
Topiramate comes in 25 mg, 100 mg and 200 mg sizes.
Begin with 25 mg bid and build if necessary to
up to 400 mg daily. Tiagabine has small milligram
sizes with the starting dosage of about 4 mg daily
and the usual dosage of 12 through 40 mg per day.
Both drugs are useful as adjunctive therapy in
patients whose seizures are uncontrolled on monotherapy
particularly in partial seizures. Side-effects
for both are rather typical for anticonvulsants
namely fatigue and psychomotor impairments.
3. THE BIOLOGICAL SLEEP CYCLE DISRUPTION:
Sleep disorders
One of the most common complaints after CHIT is
sleep disturbance which may take months or years
to fully improve. Many such complaints may be
psychiatrically linked, however, some may have
biological bases, linked with the conditions above.
Sleep disorders are among the most fundamental
of all psychiatric disorders, and certain psychiatric
illnesses may well have a very profound base with
regard to sleep disturbance. For example, a diagnosis
of mania may be nearly impossible without a profound
decrease in total sleep time and, in fact, most
manics have a period of at least 36 hours where
they do not sleep at all and during which they
do not feel fatigued (Tucker, Neppe, 1988) Similarly,
a shift with phase advance and a decreased latency
to rapid eye movement sleep is characteristic
of a biological depression. Another common symptom
in this condition is terminal insomnia - early
morning waking. This may or may not be correlated
with this phase advancement as the two have not
been investigated (Tucker, Neppe, 1988).
Sleep disturbance is of profound
importance in the CHIT but may reflect underlying
affective disorder or personality. Many patients
with profound degrees of antisocial personality
give a history of sleep disturbance involving
paroxysmal wakenings since childhood. Many brain
impaired individuals may have periods during which
they nap during the day.
HYPNOTICS: When sleep is impaired
significantly hypnotics may be considered. Options
include zolpidem (FDA approved), trazodone (approved
as antidepressant but commonly used) and melatonin
(non-prescription hormone)
a. ZOLPIDEM TARTRATE (AMBIEN) medication.
This is a imidazopyridine nonbenzodiazepine hypnotic
with no apparent dependence, and normalization
of sleep cycles with extensive European experience
(5 mg pink or 10 mg white tabs - breakable). It
acts at the omega 1 sites of GABA - a receptor
preferentially. It is FDA indicated for short-term
management of insomnia. It has rapid onset, and
short half life (2-3 hours).
b. TRAZODONE (DESYREL) medication.
Trazodone is marketed as an antidepressant: it
does not have anticholinergic side-effects and
has little cardiotoxicity. In sub-antidepressant
doses such as 50-100 mg, it is frequently used
as a hypnotic because it is sedative with little
carry-over to the next day and has excellent physiological
effects on slow wave sleep. Patients should be
warned that it may drop blood pressure and induce
tachycardia - hence they should go to bed after
taking it until they know what effects it has
on them. In males there is a rare side-effect
of priapism (1 in 8000 males) which can usually
effectively be treated with pseudo-ephedrine hydrochloride
and immediately packing the penis with ice.
c. MELATONIN: Given the biological
sleep disturbance component and disturbances in
diurnal rhythms, Melatonin is a non-prescribed
option left to the patient's choice. The following
key information should be communicated:
- the lack of research on the drug
- questions on purity of the preparations
which could lead to unusual reactions (other
health food store preparations could have
the same problem).
- interactions with other drugs
- possible long-term suppression of the pineal
(speculative only) based on other neuroendocrine
responses to, for example, thyroxin and steroid
in thyroid and adrenal suppression, which
implies tapering of the melatonin in the event
of stopping.
- other unknown effects, pharmacokinetic and
pharmacodynamic.
On the other hand, melatonin remodulation
appears physiological. This has not been prescribed
per se but is available in certain health food
stores in a 3 mg and 5 mg size. Preferable is
the smallest possible dose as physiologically
it is thought only 0.5 mg - 1 mg is necessary
in the normal person. Preparations of animal extraction
should be avoided at this point: vegetable or
synthetic melatonin may prove less risky. The
drug is best taken an hour before dusk and should
take several weeks to work fully.
d. Benzodiazepines: Benzodiazepines
should be avoided, if possible, because of their
addictive qualities and impairments at the psychomotor,
cognitive, amnesic and drug interactional levels.
The benzodiazepine may relieve symptoms non-specifically
and incompletely but has all the cognitive, psychomotor,
and dependence, addictive problems of this drug
group. This may be aggravated by previous abuse
history and symptomatic status.
e. Sleep disturbance usually appears
secondary in the CHIT and should be managed with
no napping during the day.
4. MANAGEMENT OF DEPRESSION AND
MOOD DISORDER: Affective Disorders and Head injury
The area of mood disorders allows possible practical
and theoretical understanding of the role of the
central nervous system in behavior disorders.
Affective disturbances may be triggered or induced
by head injury with or without patients with traumatic
temporal lobe epilepsy (Neppe, Tucker 1994) and
head trauma (Neppe, Tucker 1994; Tucker, Neppe
1991).
We believe that CHIT may trigger
"Depressive pseudodementia" in patients
with limited cerebral reserve (MacAllister, 1983,
1992). This refers to the organic symptomatology,
particularly dementing symptoms in affectively
disturbed patients. Cognitive and neuropsychologic
disturbances are associated with affective disturbances
generally reversible with treatment. Consequently,
in dealing with the demented patient, one must
rule out affective disturbance in the older patient
(Neppe, Tucker 1994).
a. LITHIUM CARBONATE (ESKALITH AND
OTHERS - choice is optional): occasionally lithium
is useful when patients manifest cyclical phenomena
of their residual focal CHIT. Medication problems
with lithium are linked commonly to tremor which
is a rather coarse static one which patients find
impairing in functionality and embarrassing. Some
patients become nauseous and/ or confused. Our
preference is to lower dosage in the event of
any of the above symptoms. Baseline blood tests
of electrolytes and renal functions are important
as is frequent monitoring for a major but neglected
long-term complication nephrogenic diabetes insipidus
commonly presenting as polyuria or nocturia. One
way to initiate lithium is by giving 600 mg on
the first day and check a level after 24 hours.
This will also screen for those who become Lithium
toxic rather quickly. Lithium is an extremely
lethal compound and should be used under supervision
of a psychiatrist. Two different blood levels
can be considered: Low dose with less side-effect
potential but possibly less control: aim at a
blood level of 0.4-0.6 meq / L. High dose with
more side-effect potential but possibly more control:
aim at a blood level of 0.7-0.9 meq / L. Many
colleagues use higher doses but this would not
be my preference in this instance.
b. ANTIDEPRESSANT options can be
applied in the context of mobilization of significant
or major depression either post-traumatically
or post-concussionally in the CHIT or in alleviation
of pain (not approved). Our preference is to avoid
the SSRIs group as well as the tricyclics and
to use nefazodone or venlafaxine as selective
drugs acting reasonably physiologically at the
norepinephrine and serotonin receptor levels.
Bupropion may also be of value.
b.1. NEFAZODONE (Serzone): This
antidepressant of triazolopyridine structure has
ideal theoretical elements both for agitated and
retarded depression. The reason relates to its
modulating SSRI properties which implies less
side-effects such as agitation, anxiety, sexual
related pathology, nausea, akathisia and suicidality.
It has additionally serotonin 2 blocking effects
which should enhance both antidepressant and anti-aggressive
properties and further diminish SSRI side-effects.
It is more sedative than the other SSRIs but far
less than the triazolopyridine, Trazodone. My
preference is to start with doses of 50 mg bid
and increase every 3 days by 50 mg daily, always
giving bid dosing until an initial dose of 200
mg bid is achieved. Doses should best be given
in the morning and afternoon because of its short
half life and uneven kinetics. Costs of all sizes
are equal - 200 mg, 150 mg, 200 mg, 250 mg. Serzone
inhibits the 3A4 part of Cytochrome P450 enzyme
system in the liver. This increases levels of
certain chemicals e.g. ketoconazole, alprazolam,
triazolam, and probably SSRIs like fluoxetine
as well as some calcium channel blockers. These
substances should increase Nefazodone levels as
well and a 50% dose adjustment is general rule.
Particularly, do not give with Seldane (terfenadine)
and Hismanal (astemizole) - if necessary change
to Claritin (Loratadine) (10 mg Claritin usually
equal to 10 mg Hismanal, 60 mg bid of Seldane)
b.2. Venlafaxine (Effexor) This
has the advantage of acting at both serotonin
("sledgehammer" pharmacologic) and norepinephrine
("chisel" and more physiologic) and
should not produce the sexual dysfunction of the
SSRIs. Its limitations relate to possible nausea,
escalated blood pressure and agitation. It is
logical in the retarded depressive patient.
b.3. Bupropion (Wellbutrin): This
antidepressant likely acts clinically through
a somewhat irreversible norepinephric re-uptake
inhibitor effect of an active metabolite hydroxy
bupropion and not the dopaminergic effect previously
thought. Bupropion differs from most antidepressants
in its absence of effect on serotonin. Given the
availability of a long-acting form, twice daily
dosing is logical with a starting dose of 75 mg
twice per day building if necessary to 300 mg
daily. Likely choice is based on amotivation,
the norepinephric effect supplementing serotonergic
drugs if necessary, lack of sexual dysfunction,
overweight status, and need for some activating
action.
b.4. In our opinion, the following
antidepressants are not usually recommended in
the CHIT patient with depression, but are commonly
prescribed by some - the tricyclic antidepressant
and the selective serotonin re-uptake inhibitor
groups. I. Tricyclic antidepressants like nortriptyline,
imipramine and desipramine. The tricyclic group
has problematic side-effects namely potential
epileptogenicity, memory impairments, cardiotoxicity
due to arrhythmias, anticholinergic effects such
as urinary retention, dry mouth, blurred vision
and constipation, interaction with alcohol, and
sedation. In the CHIT patient, the dysmnesic and
seizure elements are particularly troublesome.
NORTRIPTYLINE (Aventyl, Pamelor)
medication. This tricyclic antidepressant is potent
and can be used frequently in doses of 75 mg per
day in instances requiring 150 mg of similar other
tricyclic agents. Moreover the monitoring of blood
levels to an antidepressant therapeutic window
allows easy evaluation particularly in the complex
patient on carbamazepine. Its effects are predominantly
serotonergic.
IMIPRAMINE (Tofranil) medication
for biological depression is linked with seizures
This is two-edged as it may exacerbate seizure
phenomena. This tricyclic antidepressant is potent
and can be used frequently in doses of 75 mg-150
mg per day in this case. Its effects are predominantly
adrenergic.
DESIPRAMINE (Norpramin) medication.
This tricyclic antidepressant is not very potent
mg for mg and is used frequently in doses of 150-225
mg per day. It is a breakdown product of imipramine.
In practice, it is more activating, less sedating
and causes more sweating than the more sedative
tricyclics. Its effects are predominantly noradrenergic.
II. Selective Serotonin Re-uptake
Inhibitors (SSRIs) like fluoxetine, paroxetine
and sertraline. This group of drugs do not have
the anticholinergic nor cardiotoxic side-effects
of the tricyclic antidepressants. However, they
are potent serotonergic agonists with no way to
diminish the effect other than breakdown of active
compound. These drugs have two problematic common
side-effects namely nausea and sexual dysfunction.
They may paradoxically increase anxiety, irritability
and agitation, accentuate nausea and disrupt sleep.
There is a possible discontinuation syndrome,
and clinically frequently loss of effects, or
need for escalating dosage occurs over time and
it is for these reasons particularly that we do
not recommend the SSRIs to the CHIT patient. The
serotonergic effects of all the current SSRIs
appear non-specific on supposedly all serotonin
receptor subtypes. As such, the risk of paradoxic
reactions is theoretically higher.
FLUOXETINE (Prozac) with its extraordinarily
long half-life (>400 hours including the metabolite
norfluoxetine) should be used with extreme caution.
In fluoxetine particularly there is controversy
surrounding precipitation of suicidality, aggression,
akathisia and tardive dyskinesia.
PAROXETINE (Paxil) does not have
an active metabolite but it inhibits the hepatic
P450 cytochrome enzyme system. It has a one day
half life. Start with doses of 20mg per day initially
and later 30 mg per day built up as necessary
to 50 mg per day. SERTRALINE (Zoloft) has a minor
probably non-significant active metabolite. We
now know that it does effect the hepatic P450
cytochrome enzyme system so there may be drug
interactions. It has a slightly longer half life
than paroxetine - several days. Start with doses
of 25 mg per day (half of 50 mg tablet) initially
for three days and then 50 mg per day built up
as necessary to 100 mg per day.
MORE UNCOMMON PHARMACOLOGIC OPTIONS
FOR THE CHIT PATIENT
1. PHYSIOLOGIC RESTABILIZATION
by BETA-BLOCKADE if numerous somatic - bodily
- symptoms exist may be considered. NADOLOL (CORGARD)
medication. Beta-blockers are useful in this instance
for the somatic features of anxiety and agitation.
They are not specifically FDA approved for these
indications. Nadolol is suggested as the only
poorly lipid soluble broad-spectrum (B1 and B2)
beta-adrenergic blocker which can act peripherally
and because of lack of intrinsic sympathomimetic
activity can be dosed according to pulse. The
dose is similar to that of propranolol (Inderal).
The initial starting dose usually suggested is
half 20mg tablet t.i.d. i.e. 10 mg t.i.d. We suggest
this be built up gradually by increasing by 10
mg every 3 days to a initial aim level of mg per
day. The drug should be administered as a t.i.d.
dosage and was chosen over other beta-blockers
because it is not very lipid soluble (avoiding
central side-effects), has both beta1 and 2 effects
and has no intrinsic sympathomimetic activity
so that an initial titration of dose to a pulse
of 66/ minute can be aimed at. Important side-effects
relevant for the patient include:
- Precipitation of asthma, diabetes, hypotension,
cardiac failure and peripheral vascular disease
leading to these conditions being contra-indicated.
- The awareness that too much is being taken
if the pulse goes into the fifties.
- To contact the treating physician if signs
of cardiac failure such as pedal edema develop.
If the response to the nadolol is
partial, we suggest changing to a lipid soluble
betablocker - to propranolol (Inderal) and building
up to a dose of about 480 mg per day or till side-effects
or till pulse is = 60/minute. The change around
from nadolol can be mg for mg and direct substitution
from 40 mg t.i.d. nadolol to 40 mg t.i.d. of propranolol.
Thereafter maintain the dose for 1 week and increase
by 20mg t.i.d. more per week till 120 mg qid or
pulse = 60/min pre-dosage or side-effects such
as dizziness (Neppe, 1989 C).
2. PSYCHOSTIMULANTS are occasionally
worth considering in the CHIT particularly in
the context of residual focal non-episodic phenomena
and / or a history of paradoxic responses. These
drugs should be used with caution based on potential
dependence, misuse (also by others), tics and
possible tachyphylactic effects. One approach
is to use these drugs in both attention deficit
disorder and narcoleptic syndromes as provocative
pharmacologic tests: non-response without side-effects
= increase the dose; worsening = take patient
off; improvement = maintain.
One preference is generally for
the scheduled methylphenidate (Ritalin) which
appears more effective than pemoline (Cylert)
(which requires liver function tests six monthly)
but requires bid or tid dosing; it should also
be safer than dextro-amphetamine sulphate (abuse
potential, possible potential to a "model
psychosis" / paranoid syndrome). Start with
10 mg qd and build up to 10 mg tid initially over
10 days. The patient should record responsiveness.
A second preference is for pemoline
(Cylert) (which requires liver function tests
six monthly) but is less highly scheduled, less
likely to be abused? and cause tics? and can be
given daily but it may be less effective than
methylphenidate (Ritalin); it should also be safer
than dextro-amphetamine sulphate (abuse potential,
possible potential to a "model psychosis"
/ paranoid syndrome). Start with 37.5 mg qd and
build up to 75 mg qd initially over 10 days. The
patient should record responsiveness.
3. ANTIPSYCHOTIC USE: Psychotic
Disorders and Head injury
There are many neurologic causes of psychosis
(Table 1), particularly seizure disorders and
more so complex partial seizures (or temporal
lobe epilepsy). This may be a possible link of
the rare onset of paranoid psychosis after brief
traumatic brain injury. In 1963, Slater and Beard
pointed out that all of the symptoms that have
been observed in schizophrenic patients can occur
in patients with seizure disorders. Recent efforts
using standardized diagnostic rating scales have
shown that the positive symptoms of the psychotic
state of patients with temporal lobe seizure disorders
is almost identical to schizophrenics (Trimble,
1982; Toone, 1981). Seizure disorders present
with a high incidence of behavioral disturbance,
which may initially be interpreted as psychiatric
in origin (Neppe, Tucker, 1994). The range of
behavioral symptoms is listed in Table II and
most patients have only one or two of these symptoms
that remain consistent over the course of the
illness. (Neppe, 1989 D)
NEUROLEPTICS (antipsychotics; also
called major tranquilizers) should be avoided
in the head injured as there is a higher risk
of tardive dyskinesia (Neppe, Holden, 1989; Neppe
1989 D). Exceptions relate to the very occasional
presence of or exacerbation of psychosis. PERPHENAZINE
(TRILAFON) medication has become our preferential
drug in post-traumatic psychosis as part of the
residual focal elements of the CHIT. Perphenazine
is approved for use in psychotic conditions. Amongst
the important side-effects discussed is the long
term risk of tardive dyskinesia and related syndromes
and its relevance to diagnosis, dosage, duration
of treatment, smoking epidemiology and the limited
amounts of treatment. Anticholinergic medication
is sometimes prescribed to alleviate the extra-pyramidal
side-effects of neuroleptic drugs. The patient
should not routinely receive anticholinergic agent
with the perphenazine as this complicates pharmacokinetics,
may accentuate psychosis, is usually unnecessary
and disputably increases the risk of tardive dyskinesia.
Additionally, anticholinergics mask neuroleptic
dosage somewhat. Also, additional potential side-effects
of dry mouth, dilated pupils with blurring of
vision, constipation, confusion, memory impairment
and delirium may occur (Neppe, Ward, 1989). When
there is a previous history of response to anticholinergics
but with side-effects of sedation, an anticholinergic
which is relatively non-sedative, has low abuse
potential, and which moreover has some muscle
relaxant effect, orphenadrine (Norflex) is recommended.
Usual doses are 50 mg TID. If not tolerated, lower
doses can be tried. A maximum of 100 mg tid should
be used. The most commonly used anti-Parkinsonian
anticholinergic in the USA appears to be benztropine
(Cogentin).
4. SPECIAL REPLACEMENT OF VITAMINS,
MINERALS AND FATTY ACIDS. This is speculative
only:
a. ANTI-OXIDANTS A recent area of
some interest, theoretical speculation and difficulty
appreciating cause-effect relationships and consequent
therapeutic efficacy is the use of anti-oxidant
medications in instances of neuronal or neurologic
diseases including pervasive developmental disorder,
Landau-Kleffner syndrome, atypical epilepsies,
multiple sclerosis, and mental retardation. These
organic brain conditions may or may not prove
to have end point biochemical similarities with
CHIT. Anti-oxidants should be considered if the
profile includes abnormal glutathione enzymes
like Glutathione peroxidase and transferase, and
various trace elements like Selenium plus a Lipid
peroxide index. These cannot be measured but speculatively
may be abnormal in a CHIT with residual or post-concussional
elements. The following guidelines are thought
appropriate at this time:
RX Medication |
size |
Dosing |
comments |
Vitamin C |
1500 mg long acting |
1500 mg BID Or Daily |
|
Vitamin E as D tocopherol |
400 iu |
400 iu BID |
use d isomer of tocopherol if possible |
Selenized yeast |
100 ug Selenium |
100 ug BID |
This is thought to be toxic beyond doses
of 800 ug per day |
Target symptoms to monitor at are
energy, lethargy, concentration, daydreams, communication
b. MINERAL, VITAMIN, OMEGA SUPPLEMENTATION
Chromium picolinate 200 ug to 400 ug daily, Magnesium
ion e.g. as chloride 400 mg per day (with some
calcium if necessary to avoid diarrhea), and Zinc
15 mg daily and the Omega fatty acids are interesting
mineral and vitamin or food supplements in this
kind of patient. There is limited uncontrolled
or anecdotal or lay literature suggesting this
combination may assist potential towards hypoglycemia
and may allow weight control (particularly chromium
based on its controversial effect in relation
to glucose cell utilization and possibly zinc),
lower risk of heart attack (magnesium particularly)
and diminished seizure risk (magnesium and secondarily
chromium). Obviously, such supplementation is
unnecessary in some but as it is not easy to distinguish
in any particular case, and the patient may wish
to explore these possibilities ensuring that the
best quality brands are bought and knowing that
besides risks linked with the vehicles containing
these medications (as with any vitamin or mineral
or sometimes generic type medication) there may
be unknown interactions occurring.
CONCLUSION:
We are doing a full circle. Cesare
Lombroso, last century wrote about the constitutional
psychopath (Lombroso, 1912). Sociologists and
behaviorist psychologists claimed that there were
no such constitutional givens and that all behavior
was socially determined totally ignoring the organism.
We have now returned to the stage where constitutional
and biologic components have again become important
and well demonstrated in our conceptualization
of transient traumatic head injury.
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TABLE 1
International League Against Epilepsy
Revised Classification of Epileptic Seizures (1981)
- Partial (focal, local) seizures:
- Simple - motor, somatosensory, autonomic,
psychic
- Complex
- Impaired consciousness at outset
- Simple partial followed by impaired
consciousness
- Partial seizures evolving to generalized
tonic-clonic (GTC)
- Simple to GTC
- Complex to GTC
- Generalized seizures (convulsive or non-convulsive)
- Absence seizures
- Atypical absences
- Myoclonic
- Clonic
- Tonic
- Tonic-clonic
- Atonic
- Combinations
- Unclassified epileptic seizures
TABLE 2: POSSIBLE TEMPORAL LOBE
SYMPTOMS (PTLSs)
Controversial PTLSs (CPTLSs)
- severe hypergraphia
- severe hyperreligiosity
- polymodal hallucinatory experience Paroxysmal
(Recurrent) Episodes of:
- profound mood changes within hours
- frequent subjective paranormal experiences
e.g. telepathy, mediumistic trance, writing
automatisms, visualization of presences or
of lights/colors round people, dream ESP,
out-of body experiences, alleged healing abilities
- intense libidinal change
- Uncontrolled, lowly precipitated, directed,
non-amnesic aggressive episodes;
- recurrent nightmares of stereotyped kind
- episodes of blurred vision or diplopia
Not Necessarily Disintegrative
PTLSs (NPTLSs)
Symptoms Not Necessarily Requiring
Treatment Paroxysmal (Recurrent) Episodes of:
- Complex visual hallucinations linked to
other qualities of perception such as voices,
emotions, or time
-
Any form of:
-
Auditory perceptual abnormality;
-
Olfactory hallucinations;
-
Gustatory hallucinations;
-
Rotation or disequilibrium
feelings linked to other perceptual qualities;
-
Unexplained "sinking,"
"rising," or "gripping"
epigastric sensations;
-
Flashbacks;
-
Illusions of distance, size
(micropsia, macroscopy), (micropsia), loudness,
tempo, strangeness, unreality, fear, sorrow;
-
Hallucinations of indescribable
modality.
-
Temporal lobe epileptic deja
vu (has associated ictal or postictal features
{headache, sleepiness ,confusion} linked to
the experience in clear or altered consciousness
)
-
Any CPTLSs which appear to
improve after administration of an anticonvulsant
agent such as carbamazepine.
Disintegrative PTLSs (DPTLSs)
Symptoms Requiring Treatment: Paroxysmal
(Recurrent) Episodes of:
- Epileptic amnesia;
- Lapses in consciousness;
- Conscious "confusion" ("clear"
consciousness but abnormal orientation, attention
and behavior);
- Epileptic automatisms;
- Masticatory-salivatory episodes;
- Speech automatisms;
- "Fear which comes of itself" linked
to other disorders (hallucinatory or unusual
autonomic) ;
- Uncontrolled, unprecipitated, undirected,
amnesic aggressive episodes;
- Superior quadrantic homonymous hemianopia;
- Receptive (Wernicke's) aphasia.
- Any CPTLSs or NPTLSs with ictal EEG correlates.
Seizure related features (SZs)
Any typical absence, tonic or clonic
or tonic-clonic or bilateral myoclonic seizures
in the absence of metabolic, intoxication or withdrawal
related phenomena.