Visuospatial and Sensory Integration Tasks in Patients With Schizophrenia or Schizoaffective Disorder: Relationship to Body Mass Index and Smoking.

Neurological soft signs (NSSs) are highly prevalent among patients with schizophrenia, but their pathophysiological significance remains unclear. The present study employed perceptual-motor and visuospatial processing tests that have not yet been attempted in this patient population. Patients with schizophrenia or schizoaffective disorder (n = 42) and mentally healthy subjects (n = 10) were administered Copy Figure Test, Detection and Recognition of an Object Test and Road Map Test. As compared to controls, schizophrenic and schizoaffective patients displayed significantly poorer ability to copy three-dimensional figures (namely, Necker- and hidden line elimination cubes) and to orient in space on a road-map test; group differences in copying two-dimensional figures and on objects' recognition against a background noise were not apparent. In the schizophrenia/schizoaffective group, more mistakes on the hidden line elimination cube was associated with greater body mass index and greater severity of nicotine dependence measured via the Fagerstrom Test of Nicotine Dependence. The above findings replicate those of prior reports and extend them to the tasks that do not involve motivational and attentional confounds. Furthermore, the present data support the hypothesis that subtle cerebral cortical abnormalities detected with specific NSSs tests may be related to some aspects of metabolic and motivational function in patients with schizophrenia/schizoaffective disorder.

Pilot Study of Neurological Soft Signs and Depressive and Postconcussive Symptoms During Recovery From Mild Traumatic Brain Injury (mTBI).

Neurological soft signs (NSSs) tap into a variety of perceptual, motor, and cognitive functions. The authors administered a battery of NSSs serially to a group of 14 pilot patients recruited from an emergency room after they experienced a mild traumatic brain injury. Patients were seen within 96 hours after injury, and again 30 and 90 days later. Measures of balance, mood, and postconcussive symptoms and impairment were also obtained. NSSs and balance improved across visits. Across visits, NSSs and balance were not significantly associated with any postconcussive outcome measures, although depressive symptoms were. Initial neurological impairment appeared to predict subsequent residual postconcussive symptoms and impairment, but this result requires replication.

Neurological soft signs in individuals with pathological gambling.

Increased neurological soft signs (NSSs) have been found in a number of neuropsychiatric syndromes, including chemical addiction. The present study examined NSSs related to perceptual-motor and visuospatial processing in a behavioral addiction viz., pathological gambling (PG). As compared to mentally healthy individuals, pathological gamblers displayed significantly poorer ability to copy two- and three-dimensional figures, to recognize objects against a background noise, and to orient in space on a road-map test. Results indicated that PG is associated with subtle cerebral cortical abnormalities. Further prospective clinical research is needed to address the NSSs' origin and chronology (e.g., predate or follow the development of PG) as well as their response to therapeutic interventions and/or their ability to predict such a response.

Impaired reproduction of three-dimensional objects by cocaine-dependent subjects.

This study employed a perceptual-motor task of figure copying in 27 cocaine-dependent, 26 marijuana-abusing or dependent, and 33 healthy subjects. Cocaine-dependent and healthy individuals did not differ in their scores on the copying of a two-dimensional diamond and a cross. In contrast, cocaine-dependent subjects displayed significantly poorer ability to copy a three-dimensional Necker cube, a smoking pipe, a hidden line elimination cube, a pyramid, and a dissected pyramid. Marijuana users' performance on all copied figures was comparable to that of the healthy comparison subjects. Considering that decreased three-dimensional copying ability has been found to be associated with fatal injuries, further studies are needed to investigate possible underlying mechanisms (e.g., parietal lobe damage) and their role in the pathophysiology of cocaine dependence.

Configural cue performance in identical twins discordant for posttraumatic stress disorder: theoretical implications for the role of hippocampal function.

BACKGROUND: A significant subgroup of individuals with posttraumatic stress disorder (PTSD) exhibits chronic, unremitting symptomatology that has also been associated with smaller hippocampal volume. The hippocampus plays a significant role in configural processing of contextual cues that facilitates context-appropriate extinction of conditioned fear. We test the hypothesis that hippocampus-based configural processing deficits are a pre-existing vulnerability factor for unremitting forms of PTSD. METHODS: Participants included male monozygotic twin pairs who were discordant for combat trauma. In 18 twin pairs the combat-exposed brother developed unremitting PTSD, whereas in 23 pairs the combat-exposed brother never developed PTSD. Participants were compared in the capacity to solve allocentric spatial processing tasks, and this performance was examined for its relationship to the severity of PTSD symptomatology and hippocampal volume. RESULTS: Although not completely differentiated from overall IQ, PTSD combat veterans demonstrated significantly impaired performance in configural processing relative to non-PTSD combat veterans. Despite having neither combat-exposure nor PTSD, the unexposed co-twins of combat veterans with PTSD displayed the same decrements as their brothers. Deficits were significantly related to PTSD severity and hippocampal volume. CONCLUSIONS: The current study provides the first evidence that the relevance of the hippocampus in PTSD might be related to pre-existing configural cue processing deficits that predispose individuals to develop unremitting forms of the disorder.

Clarifying the origin of biological abnormalities in PTSD through the study of identical twins discordant for combat exposure.

A biological abnormality found to be associated with posttraumatic stress disorder (PTSD) may be, among other things, a pretrauma vulnerability factor, that is, it may have been present prior to the event's occurrence and increased the individual's likelihood of developing PTSD upon traumatic exposure. Alternately, it may be an acquired PTSD sign, that is, it may have developed after the traumatic exposure, along with the PTSD. We have studied pairs of Vietnam combat veterans and their noncombat-exposed, identical twins in an effort to resolve these competing origins. Combat veterans were diagnosed as current PTSD or non-PTSD (i.e., never had). Average heart rate responses (HRRs) to a series of sudden, loud-tone presentations were larger in Vietnam combat veteran twins with PTSD, but these larger responses were not shared by their noncombat-exposed cotwins, whose responses were similar to those of the non-PTSD combat veterans and their noncombat-exposed cotwins. These results suggest that larger HRRs to sudden, loud tones represent an acquired sign of PTSD. In contrast, increased neurological soft signs (NSSs), diminished hippocampal volume, and presence of abnormal cavum septum pellucidum (CSP) were found in Vietnam combat veteran twins with PTSD and their "high-risk," unexposed cotwins compared to Vietnam combat veteran twins without PTSD and their "low-risk," unexposed cotwins. These results support the conclusion that the latter abnormalities represent antecedent, familial vulnerability factors for developing chronic PTSD upon exposure to a traumatic event.

Neurocognitive function in monozygotic twins discordant for combat exposure: relationship to posttraumatic stress disorder.

Neuropsychological deficits have been reported among trauma survivors with posttraumatic stress disorder (PTSD). It is often assumed that these cognitive difficulties are toxic consequences of trauma exposure. Alternatively, they may reflect preexisting characteristics that contribute to the likelihood of developing PTSD. To address this possibility, the authors evaluated cognitive performance in monozygotic twin pairs who were discordant for combat exposure. Pairs were grouped according to whether the combat-exposed brother developed PTSD. The combat-unexposed cotwins of combat veterans with PTSD largely displayed the same performance as their brothers, which was significantly lower than that of non-PTSD combat veterans and their brothers. The results support the notion that specific domains of cognitive function may serve as premorbid risk or protective factors in PTSD.

Subtle neurologic compromise as a vulnerability factor for combat-related posttraumatic stress disorder: results of a twin study.

CONTEXT: Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. OBJECTIVE: To resolve competing origins of increased NSSs in PTSD, namely, preexisting vulnerability factor vs acquired PTSD sign. DESIGN: Case-control study of identical twins. SETTING: A Veterans Affairs and academic medical center (ambulatory). PARTICIPANTS: A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. INTERVENTIONS: Neurologic examination for 45 NSSs. MAIN OUTCOME MEASURE: Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. RESULTS: There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis x exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The "high-risk," unexposed co-twins of the former also had significantly higher NSS scores than the "low-risk," unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. CONCLUSIONS: These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial vulnerability factor for developing chronic PTSD on exposure to a traumatic event.

Performance on visuospatial copying tasks in individuals with chronic posttraumatic stress disorder.

The ability to copy figures was evaluated in 41 subjects with chronic posttraumatic stress disorder (PTSD) and 27 trauma-exposed, non-PTSD comparison subjects. Individuals with PTSD demonstrated significantly impaired performance. However, after adjusting for pre-trauma variables, there was only a marginally significant association between figure-copying performance and PTSD. These findings are consistent with pre-trauma visual-spatial impairment as being among the risk factors for chronic PTSD.

Absence of selected neurological soft signs in Vietnam nurse veterans with post-traumatic stress disorder.

This study examined eight neurological soft signs (NSSs), which had previously proved successful in discriminating medication-free post-traumatic stress disorder (PTSD) from non-PTSD combat veterans and sexually abused women, in 82 unmedicated female nurse Vietnam veterans, 32 with and 50 without PTSD. The increased NSSs observed in the previously studied PTSD samples were not found in the nurses with PTSD. The results fail to support the hypothesis that the stress of a traumatic event and/or resultant PTSD damages the nervous system.