Data of the Evaluation of Psychiatric Sphere
According to proper and the wife, being also our opinion,
based on the evaluation, the patient presents a semiologic
set of factors that must be taken in consideration.
Since its military demobilization (1974) and subsequent
return to Portugal, the patient suffers of:
A. Post-Traumatic symptomatology characterized by: a.
permanent state of agitation and hypervigilance:
“any small noise”
makes him to wake up frightened and in a state of anxiety
and considerable fidget, being difficult to come back to
sleep. Even in a vigile state, during the day, the same
situations of occurrences of intense noises produce an
immediate state of typical behaviour of war veterans: he
becomes scared, is verified high anxiety, becomes verbal and
physically more aggressive than his normative
habitual, etc. b. currently, any behaviour of others
interpreted for the patient as aggressive generate in
himself stormy behaviours, as “to argue with friends,”
shoot chickens for the soil,”
(presently the patient works in a mini-market being the
commercialisation of baked chickens one of the main
“deals with the customers in an impatient and rude form,
almost every day,” “feel strongly irritated with the
conductors of other vehicles in an exacerbated way,” “cries
out with the people,”
etc. c. intermediate insomnias (in the middle of the night),
being difficult to come back to sleep, occurring about two
times per week. Sometimes, after waking up, is not able to
return to the bed and sleep, being waked till morning.
Sometimes, as he perceives that will not come back to sleep
it rambles for the house or it wakes up the wife starting
quarrels without any rational and factual reason.
B. It presents Social Isolation since to some years, with
C. Had to the related traumatic state, he relates that it
started, about 7 years ago, to present a pattern of daily
alcohol consumptions (5 to 10 beers, 2 - 3 cups of wine in
all the meals, and for times, 3 - 4 times per week, the
ingestion of an average dose of Whisky). He still relates
that this standard of consumption leads him to commit
alcoholic abuses (“especially to reduce the anxiety”)
about two times per week, reaching to a state of light to
moderate drunkenness (“it is the only form to feel more
and not annoy me with other people nor to scare me with
things… with the noises,” “every day I am scarred...
therefore the strong noises makes me to remember the
explosions of the war”).
D. In what concerns to the personality sphere, disinhibition
is still well verified. The patient presents pre-frontal
dysfunction with considerable alterations in the field of
verbal aggressiveness and difficulty to impulse control
(without acting out) as well as reduced capacity of
frustration resistance. It must be taken in consideration
the cited in the points “A.a” “A.b” and “B.”
E. In the sphere of humour appeared being dysthymic since
about two years, anhedonia, bradyphrenia, social isolation
and sexual difficulties.
F. In the sphere of anxiety disorders, criteria Generalized
Anxiety Disorder, Serious type, are fulfilled. G. He still
presents general medical conditions as, visual difficulties,
auditory difficulties with alterations of the vestibular-
ochlear system, which produces erratic walking and strong
impeditive vertigos considering a normative pattern
functioning labour abilities.
Integration and Diagnostic Conclusion
The patient presents temporal disorientation, with fast
dysfunction of spatial functions, presenting gradual deficit
of the mnesic functions with strong socio-labour and
Of the point of view of the capacities mediated for the
cortical frontal regions the patient discloses performances
typical of social disinhibition, difficulties in controlling
the impulses and low frustration resistance. He still
presents difficulties of memory, programming and attention
due the deficit of the mechanisms regulated for the central
executive, causing a state of daily disorientation to some
levels (temporal, spatial, personal organization, etc). So,
cortical damages with marked dysfunction at the level of the
frontal lobes is verified, and less accented (but
significant) to the level of the parietal, occipital,
temporal cortical ridges.
Concernment with War Post-Traumatic Stress Disorder he also
presents Psychiatric Pathology, with association, as a
result of, or in comorbidity, with significant pathology to
the level of Generalized Anxiety, Dysthymic Mood, Antisocial
Behaviour, Generalized Aggressiveness, Personality Disorder,
Sleep Disorder and significant and continued Abuse of
Having in account the age of the patient (60 years), and the
picture presented by neuropsychological evaluation
(complemented by CAT analysis), is fortified the diagnosis
of gradual progressive dementia process of cortical
aetiology, specially, Frontal and/or Fronto-Temporal
dementia, in his first stages.
So, as the therapeutic plan for this patient, and
considering that at this moment he doesn’t have any
medication support, we consider that he would start, in
short time, consultation with a neurologist and then to be
submitted for an urgent psychiatric treatment, representing
actually a moderate risk for the safety of his proper person
or others. The patient continues to be followed by our team
Discussion and Integration of Literature
The interest of this case is related with the fact that,
since the beginning of evaluation sessions, we realized that
we were in front of a patient with a particular comorbidity.
The relationship between PTSD and cerebral damage is well
known.15-17 Nonetheless, this case looks very particular
because of the apparent aetiology of the cerebral damage
(degenerative fronto-temporal dementia) and associated
neuropsychological and neuropsychiatric symptomatology.
Some of the most studied neural circuits associated with
PTSD are hipocampal atrophy17 and syndromatic amigdalar
malfunction,18,19 frontal-limbic structures abnormalities,
18 hipoperfusion of striatum, bilateral anterior
and right orbito frontal cortex 79 and large cava
We have stated that the patient of this study presented a
considerable deficit in the cortical-sub-cortical circuits
surrounding the pre-frontal and temporal cortex (apart from
the other neuroanatomical regions cited before). Related
with this, Shin, Orr, Carson, Rauch, Macklin, Lasko, et
al.21 edited a study that could help us to understand the
neuroanatomical subjacent circuits. In a case-control study,
they tried to evaluate the potential role of the amygdala
and medial prefrontal regions in PTSD, given a special
attention to the functional relationship of the mentioned
circuits. According to the authors, the main objective of
the study was “To examine the relationship between
amygdala and medial prefrontal regions during symptom
provocation in male combat veterans (MCVs) and female nurse
veterans (FNVs) with PTSD.”
(p. 168). The sample comprised only Vietnam Veterans:
17 volunteer (10 women and 7 men), with PTSD (PTSD sample)
and 19 (10 women and 9 men) without PTSD (control
sample). Utilizing positron emission tomography and
study of the cerebral blood flow at the moment of
and neutral events.”
The authors concluded that there is a “reciprocal
relationship between medial prefrontal
cortex and amygdala function in PTSD and opposing
associations between activity in these regions and symptom
severity consistent with current functional neuroanatomic
models of this disorder.”
Summarizing PTSD models of arousal deregulation implicate
dysfunction in an inhibitory gating mechanism in the
When we use the term War PTSD, and considering the
alterations since the first scientific approach to the
theme24 as well as the first psychoanalytics clinical
descriptions,25 we are talking about, according with
American Psychiatric Association (2000) in the
“Diagnostic and Statistical
Manual of Mental Disorders”(4.Ed.,
Text Revision)5 and
“The American Heritage.”26
“A psychological disorder affecting
individuals who have experienced or witnessed profoundly
traumatic events, such as torture, murder, rape, or wartime
combat, characterized by recurrent flashbacks of the
traumatic event, nightmares, irritability, anxiety, fatigue,
forgetfulness, and social withdrawal.”
Our patient allegedly presents symptomatology of PTSD since
his demobilization from the Portuguese army in 1975. So, why
this symptomatology keeps present for the last 40 years, and
why the same symptomatology suffered a worsening in the last
two-three years? In a clinical research with 61 Holocaust
survivors, Barak & Szor27 found that, 50 years after the
Nazi regimen, 91,8% of the survivors presented a strong
diagnosis of PTSD. If we don’t consider the special
features from Holocaust phenomena, other authors suggest
that the incidence of PSTD many years after the major
war events present percentages in the order of 12.4%28
to 45%29. Once our patient is Portuguese, the citation of a
large study on PTSD occurrence30 is of great
importance to percept the frame of the Portuguese reality.
It’s estimated that about 800.000 male combatants was
exposed to trauma in the colonial Portuguese wars
between 1961 and 1975. From those, about 140.000 are
estimated as suffering from any kind of chronic
psychological problem, and particularly, the authors
concluded that the estimation for Portugal for War PTSD to
the colonial veterans are 10,9%. It’s clear then that
the prevalence of War PSTD is a considerable health issue
and the incidence may appear only several years after the
traumatic major events.
In particular, our patient appears to be developing a fronto-temporal
syndrome, with the possibility to have to be diagnosed in
the future as a Fronto-Temporal Dementia. According to Neary,
Snowden, Gustafson, Passant, Stuss, Black, et al.31
three clinical syndromes exist that suggest degeneration of
frontal-temporal regions, namely, Frontal- Temporal Dementia
(FTD), expressed by behaviour disinhibition, impulsiveness,
strong alterations in social relationships and
executive deficits. Our patient presents the FTD
disinhibited type formulated by Caixeta & Nitrini.32
This could be supported by the accepted idea that acute and
recurrent stress events can in fact produce
neurodegenerative disorders.33,34 The CAT of the
patient clearly shows atrophy of frontal poles and
disseminated by other regions and structures like the
temporal ones. The FTD was first known as Pick’s Dementia.35
It’s characterized by grey and white substance atrophy at
the frontal lobes and temporal poles and in some cases could
be widespread, affecting parietal regions (as in our
patient) and striatum, thalamus, amygdala and
hippocampus.36 The patient of our study presents a set of
characteristics presented by Allegri, Harris, Serrano &
Delavald37 as golden marks of FTD: a) Principal diagnostic
traces: insidious beginning and slow progression, lost of
respect by social rules and self care (e.g. hygienic
habits), rigidity and lack of mental flexibility, violent
and inconvenient behaviours, distractibility, impulsiveness
and impersistance, low insight about himself and other
actions and consequences; b) in terms of emotional signs, he
presents high level of anxiety and moderate depressive
symptoms, as well as anhedonia (emotional
indifference, apathy and lack of sympathy and empathy).
The reference of neuropsychological data related with PTSD
is not so common as the first relation (PTSD and Brain
alterations) although, sufficiently developed. Some classic
papers like The Neuropsychology of Anxiety: An Enquiry
Into the Functions of the Septohippocampal System,38
presents the well broad known relation between stress and
anxiety disorders and neuropsychological malfunction.
Other authors39-42 present a particular interest in the
study of traumatic stress (PTSD) and neuropsychology as well
as Friedman43 and Doblin44 with the study of neuropsychology
and neuropsychopharmacology and PTSD. However, some
studies45 present particular neuropsychological deficits in
Prisoners of War (POW) in memory, attention, and executive
deficits. Considering POW’s of the World War II, Marsella,
Friedman & Spain80 and Jacobs & Iacopino,46 suggest
deficits of memory and learning, and other problem-solving
limitations as well as several cognitive performance
deficits. The study of Vietnam Veterans from USA as been one
of the particular major area of interest, like the studies
of Vasterling, Duke, Brailey, Constans, Allain & Sutker47
about processes like attention, learning, memory
performances and intellectual resources.
During the process of neuropsychological evaluation and
considering our patient, we have taken into consideration
some aspects usually recommended in the evaluation of war
veterans, such as the possibility of malingering.10
Once we understand brain interconnection based on Hebbian
Rules, we quote Siegle & Hasselmo48 that states:
“Because runaway synaptic modification has implications for
disruptions in memory processes, neuropsychological testing,
which focuses on memory performance and has a history of
direction based on models of biological processes, is
expected to reveal such disturbances”
Horner & Hamner49 stated that the cognitive performance is
equally distributed even considering the variety of possible
stressors. Nonetheless, the authors revised the literature
and concluded that the War PTSD was the major cited type of
sub-category evoked in scientific papers considering the
whole field of PTSD. As in our patient, the most evident
cognitive deficits postulated by the authors were: memory,
particularly involving the immediate verbal and visual
information retrieval, and with a lower strength the
non-immediate retrieval of information; attention, in verbal
and visual modalities; and finally, executive functioning,
including problem solving skills.
Sachinvala, von Scotti, McGuire, Fairbanks, Bakst, Mcguire,
et al.,50 and Vasterling et al.,22 states that
the majority of war veterans are low educated, recurs
frequently to alcohol or medication and, as our patient,
presents an elevated tax of comorbidity. Weinstein, Fucetola
& Mollica,51 states that, in addition of all cognitive
deficits presented before “A pattern emerged of errors of
commission and intrusion,
with a tendency toward response disinhibition and intrusions
on cognitive tasks that correlated positively with
re-experiencing symptoms and negatively with avoidance/
In conclusion, in our opinion we are in front of a patient
with a particular dysfunction of the brain fronto-temporal
circuits, and related neuropsychological dysfunctions. That
could be the support of the evidence that the memory
deficits presented by him, is not so related with a semantic
syndrome, but with a frontal one. According to this, several
authors refers that the executive malfunctions, as
prospective memory,52 abstract thinking,53 mental
flexibility54 and work memory,55 have been also related with
this kind of population.
In terms of neuropsychiatric symptomatology related with War
PTSD, and parting from the example of our patient, it was
demonstrated that he shows insufficient functional outcomes
in the social life,56,57 as well as mood disorders, anxiety
problems, alcohol abuse, confusion, detachment, and
apprehension.58,59 The patient still presents negative
cognitive ruminations, inflectional anxiety, anger,
suspiciousness, low self-esteem, and less-adaptive
personality structures,60 alexytimia61 and anhedonia and
emotional numbing.62 Some authors state that this kind of
symptomatology appears to be dose-dependent, especially
somatic complaints, attentional difficulties, anxiety, and
depression. At the same time, this patient seems to try to
hide the stigma associated with mental disorder, pushing his
family to hide the problem and do not find clinical help.63
As well as in the majority of patients with PTSD he presents
insomnia recurring to the use of alcohol to induce sleep.64
Finally, as supported by the literature, psychiatric
comorbidity is a common theme in these populations,65
including PTSD and depression, and they “have substantial
functional consequences influencing resiliency in the
If, in fact, we can conclude that in our patient the
comorbidity exists, whether causally related or not, that we
should make an effort to integrate the deficits showed with
the evidences from literature. The comorbidity with physical
conditions in war veterans is well known,66 but what about
the psychiatric and neuropsychological findings in our
One of the symptoms most pressing for the dementia diagnosis
are deficits of memory that is characterized for
difficulties in learning of new information or forgetting
other already apprehended.67,68 The first type of memory
difficulty is the most frequent and in practical terms
expresses in losing objects of daily-life use (e.g.
keys of house, wallet, small objects, etc.), forget that
food are cooking, disorientation in familiar places, among
others aspects.69 The dysfunction of the executive
functioning is also frequent and can be due to cortical and
subcortical frontal regions.70 This type of functions are
important in the daily life situations and allows the
capacity of planning, initiating, sequencing, monitoring and
finishing actions and abstractly think on a problem.71 Our
patient strongly presents such difficulties.
In terms of neuropsychological impairments, what where the
major particularities evaluated by our team? A sufficiently
usual concept in the scope of the aging constitutes
cognitive impairment. This is defined as anyalteration of
the superior mental capacities, which is manifested usually
in an alteration or decrease of the abilities of the
individual. It can be reversible or chronic, and focal
(restricted to an area) or diffuse (to some levels), or
either, to affect only one isolated mental function or in
contrary, to affect a set of functions that is related
between itself.72 According to Rudolf, Ponds & Van Boxtel73
the cognitive impairment associated with the age is
initiated approximately in the 50 years and increases
gradually, affecting the functions of memory, attention,
speed of cognitive processing, planning and decision-making.
Petersen, Stevens, Ganguli, Tangalos, Cummings & DeKosky74
states that the detention of initial symptoms of dementia by
means of screening tests is pointed, with bases on the
results of some studies, insufficient. According to these
same authors, the epidemiological studies in the scope of
the aging and dementia habitually conclude three groups of
citizens: citizens with and without dementia and citizens
that do not fit in the category for dementia, although to
disclose a cognitive deficit (particularly in the memory),
but do not complete all the criteria for the dementia
diagnosis. Still according to the authors, other problem is
the utilization of screening tests for the detection of
Cognitive Impairment, like MMSE, Kokmen Short Test of
7-Minute Screen e Memory Impairment Screen.
states that these instruments are only truly liable when
utilized in samples that already presents high prevalence of
mild to moderate cognitive impairment.
In fact, only a profound neuropsychological evaluation of
this patient allowed us to verify some subtle deficits (as
well as major ones).
Beyond the evaluation contemplating an analysis of the
cognitive functions of the patient, an evaluation of the
activities of daily life was equally contemplated (basic
activities of daily life, instrumental activities and
advanced activities of daily life) as well as his
socio-familiar situation. 36 We had into consideration de
debate about the possible protective factor of pre-morbid
intellectual reservoir in the developing of
Neuropsychological deficits. Once this is not a clear and
free of doubt subject, we could speculate that the low
scholarity of our patient could be a factor of increase in
Finally, like suggested by various authors, in the process
of neuropsychological evaluation we have conjugated
information of clinical anamnesis, clinical neurological
evaluation,36 and neuroanatomic examinations (Computerized
With the utilization of the Portuguese Experimental Version
of Luria Nebraska Neuropsychological Battery77 we conclude
that the patient presents diffuse fronto-temporal syndrome
with involvement of the mnesics dimensions and maintenance
of accented poor levels of necessary attention and
concentration to daily life functioning. He presents
capacity of learning, being strongly affected by
interference mechanisms. Such aspect produces significant
damage in the labour performance and daily life social
The prefrontal medial cortex seems to mediate the response
between the hippocampus and the amygdala acting as a
modulator of stimulus reaction.78 So, the particular
pre-frontal dysfunction seems to be supporting the problems
at psychiatric level that we have related.
1. Turnbull, G. (2005). Post-Traumatic Stress Disorder. Mind
Works Professional Briefing, 3.
2. Macher, J.-P., & Crocq, M.-A. (2000). Editorial.
Dialogues in Clinical Neuroscience - Posttraumatic Stress
Disorder, 2(1), 1.
3. van der Kolk, (2000). State of the art. Dialogues in
Clinical Neuroscience - Posttraumatic Stress Disorder, 2(1),
4. Levy, M. I. (1995). Stressing the Point: Post Traumatic
Stress Disorder Claims. San Francisco: University of
California San Francisco, 1-8.
5. American Psychiatric Association (2000). Diagnostic and
Statistical Manual of Mental Disorders (4.Ed.). Text
Revision. Washington, DC.
6. Crocq, M-A. & Crocq, L. (2000). From shell shock and war
neurosis to PTSD - Dialogues in Clinical Neuroscience, 2
7. Kopelman, M. D. (2002). Disorders of Memory - Invited
Review. Brain, 125, 2152-2190.
8. Webb, M. (2005). Caregivers’ Needs Across a Cognitive
Lifetime. The Secret Life of the Brain – Adult Guide. Essay
9. Price, K. P. (1994). Posttraumatic stress disorder and
concussion: Are they incompatible?
Journal, 43, 113-120.
M. I., Giráldez, S. L., Rodrigo, A. M. L., &
Rionda, J. L. A. (2005). Malingering of Organic Illness
or Mental Disorder. Papeles del Psicólogo, 26, 99-108.
Dimitrov, M., Elpern-Waxman, M. N. J., Granetz, J., Phipps,
J. O. G. M., Milne, E., Logan, G. D., et al.
(2003) Inhibitory attentional control in patients with
frontal lobe damage. Brain and Cognition, 52, 258-270.
12. Milner, B., Petrides, M., & Smith, M. L. (1985). Frontal
lobes and the temporal organization of memory.
Human Neurobiology, 4, 137–142.
Guerreiro, M. (1993). Contributo da Neuropsicologia para o
estudo das demências. Unpublished Tese de Doutoramento,
Universidade de Lisboa, Lisboa.
14. Luria, A. R. (1966). Human Brain and Psychological
Processes. New York: Harper and Row.
15. Laney, C., & Loftus, E. F. (2005). Traumatic Memories
Are Not Necessarily Accurate Memories - In Review. Canadian
Journal of Psychiatry, 50, 823-828.
16. Glaesser, J., Neuner, F., Lütgehetmann, R., Schmidt,
R. & Elbert, T. (2004). Posttraumatic Stress Disorder in
patients with traumatic brain injury - Research article. BMC
Psychiatry, 4, 1-6.
Gilberston, M. W., Shenton, M. E., Ciszewiski, A., Kasai,
K., Lasko, N. B., Orr, S. P., et al. (2002). Smaller
hippocampal volume predicts pathologic vulnerability to
psychological trauma. Nature, October, 1-6.
A., Schaefer, M., Malta, L.S., Dörfel, D., Rohleder, N. &
Werner, A. (2006). A meta-analysis of structural brain
abnormalities in PTSD. Review. Neuroscience and
Biobehavioral Reviews, (In Press).
A.M. (2002). Neuroimaging findings in post-traumatic stress
Disorder. Review Article. British Journal of Psychiatry,
Myslobodsky, M.S., Glicksohn, J., Singer, J., Stern, M., Bar-Ziv,
J., Friedland, N., & Bleich, A. (1995). Changes of brain
anatomy in patients with posttraumatic stress disorder: a
pilot magnetic resonance imaging study. Psychiatry Research,
L.M., Orr, S.P., Carson, M.A., Rauch, S.L., Macklin, M.L.,
Lasko, N.B., et al. (2004): “Regional Cerebral Blood flow in
the Amygdala and Medial Prefrontal Cortex During Traumatic
Imagery in Male and Female Vietnam Veterans With PTSD”,
Archives of General Psychiatry, 61, 168-176.
Vasterling, J.J., Brailey, K., Constans, J.I., Borges, A. &
Sutker, P.B. (1997). Assessment of intellectual resources in
Gulf War veterans: Relationship to PTSD. Psychological
Assessment, 4, 51–59.
Shimamura, A.P., Janowsky, J.S., & Squire, L.R. (1991). What
is the role of the frontal lobe damage in memory disorders.
In Levin, H. M. Eisenberg, H. M., and Benton, A. L. (eds.).
Frontal Lobe Function and Dysfunction, Oxford University
Press, New York.
W.H.R. (1918). The repression of war experience. Lancet, 1,
Kardiner A. (1941). The Traumatic Neuroses of War. New York,
NY: Paul B. Hoeber.
American Heritage® (2000). Dictionary of the English
Language: Fourth Edition
Y. & Szor, H. (2000). PTSD among Holocaust survivors
Dialogues in Clinical Neuroscience, 2(1), 57-62.
A.3rd., Schnurr, P.P., Aldwin, C.M. (1994). Combat- related
posttraumatic stress disorder symptoms in older men.
Psychology of Aging, 9, 17-26.
M.A., Douglas, J.C., Holwill, B.J. (1993). Post-traumatic
stress disorder in Australian World War II veterans
attending a psychiatric outpatient clinic. Medical Journal
Australian, 158, 563-566.
Albuquerque, A., Soares, C., Jesus, P.M. & Laves, C. (2003).
The epidemiology of PTSD in the adult population in
Portugal. Original Article. Acta Médica Portuguesa, 16,
D., Snowden, J.S., Gustafson, L., Passant, U., Stuss, D.,
Black, S., et al., (1998). Cummings and DF Benson.
Frontotemporal lobar degeneration: a consensus on clinical
diagnostic criteria. Neurology, 51 (6), 1546- 554.
L. & Nitrini, R. (1998). Demência frontotemporal: estudo
psicopatológico de 10 casos. Revista de Psiquiatria Clínica,
25 (3), 132-134.
T., Stefano, G.B., Fricchione, G.L. & Benson, H. (2002). The
role of stress in neurodegenerative diseases and mental
disorders. Neuroendocrinology Letters, 23, 199-208.
R., Derouesné, C., Fountoulakis, K.N. & Yesavage, J.A.
(2001). Therapeutic approaches to neurocognitive disorders.
Dialogues in Clinical Neuroscience, 3(3), 191-213.
O. & Gaviria, M. (2000). Demência Frontotemporal – una
redimensíon de la enfermedad de Pick. Revista Colombia de
Psiquiatria, 36, XXIX (2), 127-154.
Bartolomé, M.V., Fernández, V.L. & Ajamil, C.A. (2001)
Neuropsicología. Libro De Trabajo. Edición 3ª, Amarú
R.F., Harris, P., Serrano, C. & Delavald, N. (2001). Perfis
Diferenciais de Perda de Memória entre a Demência
Frontotemporal e a do Tipo Alzheimer. Psicologia, Reflexão e
Critica, 14 (2), 317-324.
G. (1989). A clinical guide to the treatment of the human
stress response. Plenum Press. New York.
39. Duke &
Vasterling (2005). Epidemiological and Methodological Issues
in Neuropsychological Research on PTSD pp. 3-26 i Vasterling
& Brewin (red.) Neuropsychology of PTSD, The Guilford Press.
40. Wu, K.
K., Chan, S. K., & Ma, T. M. (2005). Posttraumatic Stress
after SARS. Emerging Infectious Diseases, 11(8 August),
Hickling, E. J., Gillen, R., Blanchard, E. B., Buckley, T.,
& Taylor, A. (1998). Traumatic brain 90 injury and
posttraumatic stress disorder: A preliminary investigation
of neuropsychological test results in PTSD secondary to
motor vehicle accidents. Brain Injury, 12, 265-274.
J.E., Pederson, L.S., & Ryan, J.J. (1989). Effects of post-traumatic
stress disorder on neuropsychological test performance.
International Journal of Clinical Neuropsychology, 11(3),
Friedman, M.J. (2005). Pharmacological approaches to
cognitive deficits associated with PTSD. In J.J. Vasterling
and C.R. Brewin (Eds). Neuropsychology of PTSD: Biological,
Cognitive and Clinical Perspectives (pp.292-325). New York:
R. (2002). A Clinical Plan for MDMA (Ecstasy) in the
Treatment of Post-Traumatic Stress Disorder (PTSD):
Partnering with the FDA. maps, xii(3 autumn ), 5-18.
P.B., Vasterling, J.J., Brailey, K., Allain, A.N. Jr.
(1995). Memory, attention, and executive deficits in POW
survivors: contributing biological and psychological factors.
Neuropsychology, 9, 118–125.
U. & Iacopino, V. (2001). “Torture and its Consequences: A
Challenge to Clinical Neuropsychology.” Professional
Psychology: Research & Practice, 32:5 (October), 458-464.
Vasterling, J.J., Duke, L.M., Brailey, K., Constans, J.I.,
Allain, A.N. & Sutker, P.B. (2002). Attention, learning and
memory performance and intellectual resources in Vietnam
veterans: PTSD and no disorder comparisons. Neuropsychology,
G.J. & Hasselmo, M.E. (2002). Using Connectionist Models to
Guide Assessment of Psychological Disorder. Psychological
Assessment, 14(3), 263–278.
M.D. & Hamner, M.B. (2002). Neurocognitive functioning in
posttraumatic stress disorder. Neuropsychology Review, 12,
Sachinvala, N., von Scotti, H., McGuire, M., Fairbanks, L.,
Bakst, K., Mcguire, M. et al., (2000). Memory, attention,
function, and mood among patients with chronic posttraumatic
stress disorder. Journal of Nervous and Mental Disease, 188,
Weinstein, C.W, Fucetola, R & Mollica, R. (2001).
Neuropsychological Issues in the Assessment of Refugees and
Victims of Mass Violence. Neuropsychology Review, 11(3
A.R., Neshat-Doost, H.T., Taghavi, M.R., Yule, W. &
Dalgleish, T. (1999). Everyday memory deficits in children
and adolescents with PTSD: Performance on the Rivermead
Behavioural Memory Test. Journal of Child Psychology and
Psychiatry, 40, 357-361.
S. & De Bellis, M.D. (2002). Neuropsychological function in
children with maltreatment-related posttraumatic stress
disorder. American Journal of Psychiatry, 159, 483-486.
Krinstensen, C.H. & Borges, J.L. (2004). Neuropsychological
impairment, juvenile delinquency, and posttraumatic stress
disorder: Na exploratory study. Annals – 1st International
Congress on Neurosciences and Rehabilitation (p.15).
Brasília,, Sarah Network of Rehabilitation Hospitals.
M.B., Kennedy, C.M. & Twanley, E.W. (2002).
Neuropsychological function in female victims of intimate
partner violence with and without posttraumatic stress
disorder. Biological Psychiatry, 52, 1079-1088.
W.H., Seeley, J.R., & Clarke, G.N. (1997). Does PTSD
transcend cultural barriers? A study from the Khmer
adolescent refugee project. Journal of the American Academy
of Child and Adolescent Psychiatry, 36, 49– 64.
Sinnerbrink, I., Silove, D., Field, A., and Steel, Z.
(1997). Compounding of pre-immigration trauma and post-
mmigration stress in asylum seekers. Journal of Psychology,
P. B., Bugg, F., and Allain, A. N. (1990). Person and
situation correlates of post-traumatic stress disorder among
POW survivors. Psychological Reports, 66, 912–914.
P. B., Galina, A. H., West, I. A., and Allain, A. N. (1990).
Trauma-induced weight loss and cognitive deficits among
former prisoners of war. Journal of Consulting and Clinical
Psychology, 58, 323-328.
P. B., Thomason, B. T., and Allain, A. N. (1989). Adjective
self-descriptions of World War II and Korean prisoner of war
and combat veterans. Journal of Psychopathology and
Behavioural Assessment, 11, 185– 92.
Fernández, V.M. (1999). Alexitimia. Elementos, 35, 25-27.
T.B., Elhai, J.D & Frueh, B.C. (2006). Anhedonia and
emotional numbing in combat veterans with PTSD. Shorter
communication. Behaviour Research and Therapy, 44, 457–467.
J., Kjellander, C., Huang, K. & Bogumill, S. (1998).
Developing cultural competency in clinical practice:
Treatment considerations for Chinese cultural groups in the
United States. Clinical Psychology, Science and Practice, 5,
Lucchesi, L.M, Pradella-Hallinan, M., Lucchesi, M. & Moraes,
W.A.S. (2005) Sleep in psychiatric disorders. Revista
Brasileira de Psiquiatria, 27(Supl I), 27-32.
K., Poole, C., Chantavanich, S., and Ohmar, K. (1996).
Burmese political dissidents in Thailand: Trauma and
survival among young adults in exile. American Journal of
Public Health, 86(11), 1561–1569.
D., Woodward, C., Esquenazi, J. & Mellman T.A. (2004)
Comparison of Comorbid Physical Illnesses Among Veterans
With PTSD and Veterans With Alcohol Dependence. Psychiatric
Services, 55, 82-85.
W., Eberle, C., Frölich, L. & Knopf, M. (2005). Memory for
Performed Actions in Dementia of Alzheimer Type: Further
Evidence for a Global Semantic Memory Deficit. Dementia
Geriatric Cognitive Disorders, 20, 381- 87.
P.E.J. & Raaijmakers, J.G.W. & Jonker, C. (2005). Early
assessment of Dementia: The Contribution of Different Memory
Components. Neuropsychology, 19 (5), 629–640.
H.E., Cappelletti, M., Davies, P.M., Jaldow, E. & Kopelman,
M. (2000). Lost for words or loss of memories:
Autobiographical memory in semantic dementia. Brain and
Language, 74 (3).
J.D.W., Hodges, J.R. & Baddeley, A.D. (1995).
Autobiographical memory and executive function in early
dementia of Alzheimer type. Neuropsychologia, 33(12),
71. Gil, R.
(2001). Neuropsicología. (p.14; 157-170). España: Masson.
M.A. & Criado, A.H. (Coords) (2002). Intervención
psicoterapéutica en afectados de enfermedad de Alzheimer con
deterioro leve. Madrid: Ministerio de Trabajo y Asuntos
W.H.M., Ponds, M.P.J., Van Boxtel, J.J. (2000). Age-related
changes in subjective cognitive functioning. Educational
Gerontology, 26(1), 67-81.
Petersen, R.C., Stevens, J.C., Ganguli, M., Tangalos, E.G.,
Cummings, J.L. & DeKosky, S.T. (2001). Practice parameter:
Early detection of dementia: Mild cognitive impairment (an
evidence-based review). Report of the Quality Standards
Subcommittee of the American Academy of Neurology. Neurology,
Petersen, R., Doody, R., Kurz, A., Mohs, R., Morris, J.,
Rabins, P., et al., (2001). Current Concepts in Mild
Cognitive Impairment. Archives of Neurology, 58, 1985-1992.
W.J. (1994). Functional imaging in dementia: an overview.
Journal of Clinical Psychiatry, 55 (l), 5-11.
L.A.C.R., Loureiro, J.M. & Silva, C.F. (2002). Versão
Portuguesa Experimental da Bateria Neuropsicológica de Luria-Nebraska.
Departamento de Psicologia e Educação. Universidade da Beira
J.F. (2005). Trastornos por estrés y sus repercusiones
neuropsicoendocrinológicas. Revista Colombiana de
Psiquiatría, XXXIV(1), 77-100.
R.M., Vicioso, A.J., Jáuregui, J.C. Aliño, J.J. -I. &
Delgado, J.L.C.(2002). PET en neurología y psiquiatría I.
PET con FDG en el estudio del SNC. Revista Española de
Medicina Nuclear, 21(5), 370-386.
80. Marsella, A. J., Friedman, M. J., & Spain, E. H. (1992).
A Selective Review of the Literature on Ethnocultural
aspects of PTSD. PTSD Research Quarterly, 3(2), 1-8.