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Psychiatry and Neurology 577

reflect a 1)OSItraunlatic stress (lisoider afl(l its interact iOn with the prcmorbid
personality. Such patients also often report an increase ifl eniotionaliiy, disturbed
aflct with depressive symptoms1 a tendency to withd raw from company, poor
memory and concentration, increased distractibility, irritability, and poor tolerance
for ordinary environmental stimuli, For example, they may complain that everyday
noise has become intolera ble. In patients with subtle hran damage, such svnipt
oms tend to hleiid with the mental symptoms of gewraized organic damage
described previously, such that unraveling the organicity of the symptomatology
becomes difficult. lThe constancy of symptomatology of a postconciissional
syndrome, with irritability, memory complaints, diz?iness, fatigue, and social
withdrawal, suggests neurological underpinim ings, but the clinical picture may,
a1tc a time, bIerd iflto a depressive clisor de, t )i a i ccognhz;Il)lc anxiety
svndroiiw such as a panic discrdcr. Often the question arises as to whether these
endtiiiiig reactions are occasioned by underlying cereb ra! damage, a view so
easily enforced in a patients mind by overemphasis on the heac injury that
originaflv sparked the vndrome. Neurological indices are usually nOrifldl.
including magnetic tesonanue imaging (MRI), and, .s tinic goes l)y, t1m chological
is opposed ) tlie curoh)gica1 flavor of tl,e svmptonis l)eCofllCS appar cut. It
eCCSS1VC depenciency develops, a somatohim disorder may be suspected, and
careful attention to the pre naumatic medical and psychiatric history vil 1 reveal
the diagnosis.

Symptoms of Regional Dysfunction


FRONTAL LOBE SYNDROMES
Although there are extensive accounts of frontal lobe syndromes13 it is surprising
how often frontal lobe damage goes unnoticed and frontal lobe symptoms are
dismissed as unimportant. The clinical characteristics of three principal frontal lobe
syndromes, as described by Cummings.6 are shown in Table 30-2, although many
patients show an admixture of symptoms, and such disc rete syndromes are rarely
observed.
One of the specific deficits of frontal lobe damage is poor irien1ton: these patients
also show increased dis rratibilii. The often present with poor memory, the

latter sometimes being referred to as forgetting to remember. Another feature of


the memory disorder is a failure to integrate events into a proper temporal
sequence, remembering what, but not when. The thinki ng of patients with frontal
lobe lesions tends to be concrete, and they may show perseveration and stereot ypy
of their responses. Perseveration, with the inability to switch lines of thought, leads
to difficulties with aridim etical calculations such as serial sevens or carryover

TABLE 30-2 Clinical Characteristics of the Three Principal


Frontal Lobe Syndromes
Orbito frontal Syndrome (Disinhibited)

Disinhibited, impulsive behavior (pseudopsychopathic)


Inappropriate jocular affect, euphoria
Emotional lability
Poor judgment and insight
Distractibility
Frontal Convexity Syndrome (Apathetic)

Apathetic (occasional, brief angry or aggressive outbursts common)


Indifference
Psychomotor retardation
Motor perseveration and impersistence
Loss o set
Stimuluc boundedness
Oiscrcpant motor and verbal behavior
Mot programming

deficits

Three-step hand sequtnce


Alter;ating orogrzms
Reciprocal programs
Rhythm tapping

Multiple loops
Poor word-list generation
Poor abstraction and categorization
Segmented appro3ch to visuos atial analysis
Medial Frontal S;9drome Akinetic)

Paucity of spontaneous movement and gesture


Sparce verbal output (repetition rny be preserved)
Lc:ier-extremity weakness and loss f sensation

lnconnence
Fm Cumrnizigs IL: Ckrucal Neuropsychiatry. Grune & Stratton, Orlando,
FL 1985, with perission

Patients have no anomia, and repetition is intact, although they may have difficulty
with spontaneous conversational and propositional speech. This sync irome is
similar to that referied to as transcortical motor aphasia and has been designated

dynamic aphasia.
Other features of fronial lobe syndromes include reduced activity, lack of drive,
and inability to plan ahead. Patients show lack of concern and often display
aimless. uncoordinated behavior. Their affect is dist urbed, with apathy, emotional
blunting, and indiffe rence. Clinically, this picture sometimes resembles that of a
major affective disorder with psychomotor retardation.
In contrast, other patients may show euphoria and disinhihition, but the euphoria is
not that of a mania, having an empty emotional quality to it. The disinhih ition can
lead to markedly abnormal and sometimes antisocial behavior. Other clinical signs
associated with frontal lobe damage include sensory inattention in the contralateral
sensory field; abnormalities of visual

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searching: echophenomena; COIiIal)tllatiOll Iiypcrp hagia: imitation behavior in

which patients literally imitate the actions of the investigator, however ina)p
ropriate they may be; and so-called utilization behavi or, an exaggerated tendency
to grope for objects and overuse them.
Some authors have distinguished between lesions of the lateral frontal and orbital
cortex. The lateral frontal cortex is closely linked to the motor structures of the
brain, and lesions in that area therefore lead to disturb ances of movement and
action, with perseveration and inertia. Lesions of the orbital areas, vliich are

linked with the limbic and.reticuJr systems, lead to disinhihit io and changcs of
afftive lite. Tht Features oF these two svncjromrs and those of the medial frontal
svnt rome are shown in Table 30-2. TI bird svniromc j3 the medial fronta1
cingaiate syndrome, which leads to an apathetic, sometimes abulic (complete lack
of will) picti ire, which, without careful consideration, ma be mistiken for a !najor
deprecive disorder.
In clinical practice. various tests are used to detect frontal lobe damage. If only
traditional neurological and neuropsychological testing is performed.
frontal lobe pathology may go unnoiced. This point cannot be overemphasized.
namely, that the traditional basic neit rongicai examination essentially seeks an
lteration o function in the parietal and occipital cortices and in general does not
reflect frontal and cinporal lobe funut ion. When the lattcr areas of the brain are
damaged, the patients motor and psychic activities at-c influe nccd, and the
resulting behavior disturbances ref iect the pathology.
Some useful tests of frontal lobe function are given in Table 30-3, fuller
descriptions being given eLsewhere.5 A number of syndromes of abnormal

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Psychiatry and Neurology 579
in such Pttuetlts that there should bc a high level of alertness to the
possibility of frontal lobe/Ijinbic system damage, and symptoms should not
be dismissed lightly. Tissue damage may be revealed by magnetic resonalice
imaging, the niore so with ncwei highresolution and tract-tracing methods.

TEMPORAL LOBE SYNDROMES


Although a variety of pathological processes affecting the
temporal lobes lead to psychopathology, most intere sti ng and l)er1LPs most
controversial are the changes of behavior that are secondary to epilepsy that
derives from the temporal lobes. This subject is reviewed in more
detail elsewhere.
Of t!w various )sycllopa(11ologies relad to epilcv, personalit disorders and
pycloses have 1Xell the subject of most dehae. A
considerable aimtmnt of Con fusion in the literature has been
created 1w the failure of various authors to use precise terminology. Thus,
with regard to personality disorder, there has been a confusion of two concepts.
The first, a holdover fron thc earlier part of the twentieth CenttLfl and the era of
psychosomatic I I1C(Ii()I1C, ielaLs to 11W idea oi disease sttseptihlr
personalities. [his concept wis (hat paiicnts with iiain pers%nalitv tyj;es iid
ccntiLutious were susceptible to various diseascsheiice, the epileptic
Iwrsl )nalitv. There are few adherents to such concepts but the second
belief is very much alive. Essent ia.e, this aew oids that patients with Cliionic
brtn
onc. especially in theit temporal lobes, mna acquire personality changes as a direct
manifestation of an orgaimic brain svndronie. The precedent for this theory was set
in the midtwentieth century by the clear deline ation of the frontal
lobe personality profiles and the discovery of behavioral changes in animals after
bilate ral temporal lobectomy, as seen in the KlverBucy syndrome. The latter
include visual agnosia, increased sexual activity, and a dect ease of anxiety and
aggress ion. This pattern is sometimes seen in patients with bilateral temporal lobe
damage, for example, after head injury, or in some dementjas such as Picks
disease, in which the amygdala is affected early.
The idea that there is a specific interictal syndrome or
personality profile of paticnLs with temporal lobe epilepsy has been most strongly
argued from the clinical point of view by Geschwind. He included hyposexuahty,
hvperreligiosity, and hypergraphia (the tendency toward extensive and compulsive
writing) as its main features. Several studies have been carried out on
hypergraphia, as reviewed by Trimble,2 and these suggest that it occurs in a small

number of patients with epilepsy, as an all-or-nothing phen omenon and is


probably more common in right-sided temporal lobe epilepsy. The writing tends to
have an obsessional stereotypic quality to it and often has
religious, moral, and philosophical content. Variations on hvpergraphia include the
hiring of a stenographer to take down extensive notes or
compulsive, repetitive painting or drawing. A different form of hypergraphia is
sometimes seen in frontally damaged patients with tiIization behavior, and
hypergraphic schizophrenic script is commonly observed, overflowir with psycjio
tic denotat ion.
Hyposexuality is the predominant theme of any chnge in sexual behavior related to
epilepsy, although there are few controlled studies, in those that have been carried
out, signifIantlv more Patients with temp oral lobe epilepsy reported hyposexuality
compared to those with generalized forms of epilepsy, with patients often reporting
a global loss of sexual interest and showing little cnccin about it. Thus, the
link between low libido and wmporal lobe dy%fun( tiomi requires further eva!
uatioi, taking jiltO accoui possible horm onal changes, which mty he noted in
patients with epilepsy. These iiiclude low free testosterone levels in male patients,
which max be melated to hepatic enzyme inducing anticonvulsant drugs or
coiscqiienc Lu a temp oral lobe foctis.
fhic rcLttioimliip between aggression anti epilcp is oii that ihis tatised
con:ider:ihie (lisagreemiwlit. There
no doubt ht aggrciv behavior is a com:iin cause of referral of ep1eptic pItients to
psychiatrists, and several authors have tried to correlate aggressive
behavi or with abnormal himbic system (especiill amvgdala) aciivic. One of the
dii flcu!ties has been iii distinguish htg the eTects of diffuse brain damage from
thu effects of more discrete limbic S stem disease. Brain imaging studies have
shown associations between thinning of the frontal cortex (especially left sided)
and amvgclala size (decreased) in patients with epilepsy presenting with extreme
aggression,3 suggesting some biological correlates, Ii keeping with the anatomical
sites implic ated in animal models of aggression. Epilepsy should never be
diagnosed in people presenting with aggress ive outbursts unless there is a clear
history of a seizure disorder, Even then, the contribution of the seizures needs
careful consideration, since ictal as opposed to postictal aggression is quite rare.

Another area of controvers has been iliat of the interictal psychoses.4 All
neurologists have encount ered acute psychotic disturbances in patients during the
peri-ictl period; on occasion, and especially in complex partial status epilepticus,
the phenonienolog can resemble a schizophrenia-like illness in its entirety.
However, the concept that patients with temporal lobe epilepsy may be more prone
to the development of interictal psychotic disorders is less recognized. The
literature emphasizes the absence of abnormal premor bid personality traits or a
family history of psyc hiatric disturbance and an overrepresentation of temp oral
lobe abnormalities. Certain phenomenological

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