Frontal Syndrome Research Articles

The neuroppsychiatry of frontal labe syndromes

The neuroppsychiatry of frontal labe syndromes

Syndrome de personnalité organique dans la sclérose en plaque et influence du stress sur les poussées

This study focuses on a sample of 35 patients who had recently suffered an attack of multiple sclerosis. They were first subjected to the so-called life stress method in order to look for a connection between life stresses and the attacks of multiple sclerosis. The sample was compared with a paired control population composed of patients recruited from admission departments and medical emergency departments. The AMDP psychopathological evaluation method was applied to the sample, to establish a characteristic mental profile of these patients. Three types of results are highlighted. First, the comparison of the event scores shows a significant difference between the population of patients suffering from an outbreak of multiple sclerosis and the control population. A connection between "life stresses" and the triggering of the outbreaks of multiple sclerosis is therefore mentioned and discussed. Second, the application of the system of the Association de méthodologie et de documentation psychiatrique brings out a mental profile common to patients suffering from multiple sclerosis, consisting of a very specific association of mood disorders: dysphoria, euphoria and mania on the one hand, and depression, anxiety and dramatization on the other, with relative anosognosia. The correlation between dysphoria, the syndrome's principal characteristic, and the event score adds another argument in favour of the connection between life stresses and the evolution of the disease. The main components of this mental profile are primarily correlated with the existence of a neuropsychology suggestive of a medial basal frontal syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Frontal Stroke Syndromes

The frontal lobe is the largest lobe of the brain, and it is thus commonly involved in stroke. Moreover, almost one in five strokes is limited to the prerolandic areas. This high frequency of anatomical involvement is in sharp contrast with the apparent rarity of clinical frontal dysfunction in stroke. It is remarkable that frontal behavioral syndromes have been rather uncommonly reported in patients with stroke as compared to patients with other diseases, such as brain tumor. This fact is paradoxical, because an acute process (stroke) is expected to yield more clinical dysfunction than a more chronic disease (tumor). A volume effect may be the main factor leading to this phenomenon. Another interesting aspect of frontal strokes is the contribution of so-called 'silent' strokes, the recurrence of which may nevertheless lead to intellectual decline and compromise recovery from another stroke with more specific neurologic dysfunction. The contribution of stroke to understanding of frontal lobe dysfunction is important, because of the focal nature of this disease, and great opportunity for clinical-topographic classification correlations. One of the first modern attempts to develop a clinical-topographic classification of frontal lobe lesions came from the school of Luria, who tried to delineate three main types of frontal lobe syndromes (premotor syndrome, prefrontal syndrome, medial-frontal syndrome). Recent anatomic correlates using MRI make it possible to improve this classification. We suggest considering six main clinical-anatomic frontal stroke syndromes: (1) prefrontal; (2) premotor; (3) superior medial; (4) orbital-medial; (5) basal forebrain; (6) white matter. Finally, another fascinating topic relates to frontal lobe symptomatology due to stroke sparing the frontal cortex or white matter. This occurs mainly in three instances: lenticulo-capsular stroke, caudate stroke, and thalamic stroke. Studies using blood flow or metabolism measurements suggest that diaschisis (frontal lobe dysfunction from a remote lesion) may play a role. We believe that this is more likely to be related to dynamic interruption of complex circuitry than to static frontal lobe deactivation.

MENTAL AND BEHAVIOURAL DETERIORATION OF CHILDREN WITH EPILEPSY AND CSWS: ACQURIED EPILEPTIC FRONTAL SYNDROME

Four children with 'epilepsy and continuous spike-wave sleep' syndrome and mental and behavioural regression were followed prospectively with neuropsychological tests, behavioural questionnaires and sleep EEG performed at regular intervals between 1 1/2 and four years of age. The children showed a pattern of behavioural and cognitive disturbances similar to that found in some developmental autistic-like disorders, but also in adult frontal syndrome. Deterioration was probably due to an unusual long-standing epileptic dysfunction involving the frontal lobes. The process is potentially reversible and seems to be the same as postulated for acquired epileptic aphasia, but in a different localization.

The orbitomedial frontal syndrome

An orbitomedial frontal syndrome is proposed, characterized by anosmia, amnesia with confabulation, Go-NoGo deficits, personality change, and hypersensitivity to pain. The orbitomedial frontal syndrome is distinct from the clinical picture that results from dorsolateral frontal damage. Aspects of orbitomedial damage have been discussed previously in isolation, but we argue that recognition of this syndrome in toto is clinically important. It appears to be associated with poor social and vocational adjustment after brain injury, and the co-occurrence of features of the syndrome provides clues to underlying mechanisms for disinhibition and confabulation in frontal lobe patients.

Parietal and occipital lobe epilepsy: a review.

There has been considerable recent interest in frontal lobe epileptic syndromes, and less attention paid to occipital and parietal epilepsies. The occipital and parietal lobes have arbitrary anatomical borders. The prinicpal seizure symptomatology includes somatosensory (paresthetic, painful, thermal, sexual, apraxia, disturbances of body image); visual (amaurotic, elementary and complex hallucinations, illusions) and other phenomena (anosognosia, apraxia, acalculia, alexia, aphemia, confusional states, gustatory, vertiginous, adversive, oculoclonic and eyelid flutter). The seizure symptoms are of varying localizing and lateralizing value and seizure discharges may spread rapidly and perceived symptoms may reflect secondary spread rather than the primary site of seizure onset. Recognized parietal and occipital epilepsy syndromes include benign epilepsy of childhood with centrotemporal spikes, benign epilepsy of childhood with parietal evoked spikes, benign occipital epilepsy of childhood, migraine/epilepsy syndromes, and epilepsy with bilateral occipital calcification. In addition, occipital and parietal epilepsy may be on the basis of any underlying structural lesion. There is frequently a poor correlation between clinical and EEG features. MRI and functional imaging often reveals underlying pathology. There have been no specific trials of different antiepileptic drugs for occipital and parietal seizures. Surgical treatment has its place, with attention to the risk of causing a fixed neurological deficit.

The orbitomedial frontal syndrome

The orbitomedial frontal syndrome

Watershed cerebral infarcts: retrospective study of 24 cases.

Twenty-four patients presenting an acute stroke with watershed cerebral infarct on CT scan or MRI were included in this retrospective study. Age was 63 +/- 14 years (mean +/- SD), and sex ratio was 2 men for 1 woman. Main clinical features were: in anterior location, lower limb weakness and frontal syndrome with transcortical motor aphasia in left lesions or spatial dyscalculia in right ones; in posterior location, brachiofacial weakness with constant quadranopsia and hypoesthesia, and Gerstmann syndrome in left lesion. There was no distinctive feature for subcortical and multiple infarcts. In bilateral infarcts, there were one pseudobulbar syndrome, and 2 pseudo brainstem syndromes with neuropsychological signs. Aetiologies were severe carotid artery disease in 14 cases, severe cardiopathy in 6, isolated cerebral angiitis in 1, essential thrombocythemia in 1, protein C deficiency with sickle cell disease in 1, and cholesterol emboli in 1 anatomical case. CBF performed in carotid artery occlusions or tight stenoses showed evidence of haemodynamic changes. Microembolic process can be proposed in the case with cholesterol emboli. Preventive treatment is discussed.

Neuropsychological indexes of a partial frontal syndrome in patients with nonfrontal gliomas.

Neuropsychological indexes of a partial frontal syndrome in patients with nonfrontal gliomas.

Neuropsychological indexes of a partial frontal syndrome in patients with nonfrontal gliomas.

Neuropsychological indexes of a partial frontal syndrome in patients with nonfrontal gliomas.

Aphasia in an artist: A disorder of symbolic processing

Abstract This paper presents a study of a prominent Polish painter who suffered from a left brain stroke resulting in hemiparesis and aphasia. His drawing abilities were preserved on the performance level but he was not able to create the highly symbolic pictures he used to paint before the stroke. A neuropsychological examination, using Luria's approach, revealed a kinetic aphasia with some features of the frontal syndrome. The patient exhibited difficulties with reproducing and developing narratives, with understanding a moral of the story as well as with connecting components of a picture into a sensible whole. He was also unable to produce new associations of a word giving a series of its derivations instead. The patient was given appropriate treatment. Samples of pictures produced before and during the illness as well as after ‘Symbolic Thought Therapy’ reflect changes occuring in his cognitive abilities. The patient's problems are discussed against a background of differences in the mode of information processing by the left and right hemispheres taking into consideration the reports of artistic productions following brain lesions. It is also suggested that apart from the left-right dichotomy we should take into account the differences in functioning of the anterior and posterior brain areas.

Positron Emission Tomography Study in Progressive Supranuclear Palsy

In 41 patients with progressive supranuclear palsy (PSP) that was diagnosed on the basis of eight clinical criteria (25 patients with all eight criteria [probable PSP] and 16 with six or seven criteria [possible PSP]), we studied cerebral energy metabolism by using positron emission tomography and the fludeoxyglucose F 18 or the oxygen 15 method. Compared with age-matched controls, each of the cortical and subcortical metabolic values was significantly reduced, with a predominance in the frontal cortex, in both groups of patients with probable and possible PSP, without a difference between these two groups, suggesting similar underlying disease. The frontal metabolic value decreased with disease duration, but the relative frontal hypometabolism (expressed as the fronto-occipital metabolic ratio) was apparently already present in the early stages of the disease. The parkinsonian motor score was correlated with the caudate and thalamic metabolic values. The intellectual deterioration index was significantly correlated with both the frontal and the nonfrontal metabolic values. Finally, the frontal neuropsychological score was significantly correlated with only the fronto-occipital metabolic ratio. Hence, in PSP, a degenerative brain disease with subcortical lesions, the prominent frontal lobe-like syndrome essentially depends on the relative hypometabolism of the frontal cortex.

Giant aneurysm causing frontal lobe syndrome

A 67-year-old patient with a completely thrombosed giant aneurysm of the anterior communicating artery is described. The only neurological findings were a disturbance of stance and gait and slight bilateral grasp reflexes. He had had the features of a frontal lobe psychotic syndrome for more than 12 years. Computed tomography demonstrated a primarily hyperdense calcified suprasellar space-occupying lesion. Magnetic resonance imaging proved valuable in establishing the correct diagnosis, which was confirmed post mortem.

Frontal cortex, timing and memory

Two sets of experiments examine the psychological functions and neural organization of the frontal lobes. The first set investigates the effects of lesions of the frontal cortex (FC) on the ability to perform temporal discriminations, using the techniques and theoretical framework of scalar timing theory. FC lesions changed the reference memory for the expected time of reinforcement, so that rats expected reinforcement later than it actually occurred. These results demonstrate that the FC modulates temporal memory. The second set of experiments examined the behavioral effects of lesions in the nucleus basales magnocellularis (NBM), an area in the basal forebrain that has a significant projection to the frontal cortex. NBM lesions produced impairments in many different tasks assessing both recent and long-term memory. A comparison of the behavioral and neurochemical effects of different types of lesions in the NBM examines the role of cholinergic and noncholinergic neurotransmitters in these behavioral deficits. These data demonstrate that a “frontal syndrome” can follow selective lesions in the NBM, and indicate that the NBM must have a strong role in frontal lobe function.

OBSESSIVE-COMPULSIVE AND OTHER BEHAVIOURAL CHANGES WITH BILATERAL BASAL GANGLIA LESIONS

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.

Frontal amnesia and the dysexecutive syndrome

This study analyzes the memory deficits shown by an amnesic patient with bilateral frontal damage and a dysexecutive syndrome. He resembles a classic amnesic patient in showing grossly impaired episodic memory for both verbal and nonverbal material, together with normal digit span, and on occasion normal recency in free recall. He differs from the classic amnesic pattern however in showing an impairment in both the speed and accuracy of performance on tests of semantic memory, and in clear evidence for impaired performance on some though not all procedural learning tasks. Finally, his autobiographical memory was poor and subject to substantial confabulation. It is suggested that the pattern of deficits is consistent with a combination of a classic amnesic syndrome with the additional problems associated with the frontal dysexecutive syndrome, rather than exhibiting a qualitatively different form of amnesia.

Neuropsychological syndromes in right hemisphere stroke patients.

A specific set of syndromes, based on different intrahemispheric lesion locations, has not yet been described in patients with right hemisphere lesions. To explore whether statistically derived clusters could give clues to a syndrome structure, neuropsychological data from a sample of 106 patients with right hemisphere stroke were studied. CT data were available for 58 of the patients. Based on factor analysis of eight test and four ratings variables, six variables were chosen for a cluster analysis. A structure of 13 clusters was considered statistically valid. Combining clusters with parallel test profiles into main cluster classes, five right hemisphere syndromes proved clinically valid: an above average syndrome (n=46), denial perseverance (frontal) syndrome (n=14). a depressed mood syndrome (n= 14), a focal RH syndrome (n=18) and a global RH syndrome (n=9). It is suggested that syndromes are related to intrahemispheric location of the lesion, such as the extent of anterior and posterior damage.

Human autonomy and the frontal lobes. Part I: Imitation and utilization behavior: a neuropsychological study of 75 patients.

A type of pathological behavior, imitation behavior (IB), is newly described. In this behavior patients imitate the examiner's gestures, although not instructed to do so. Patients explain that they thought they had to imitate the examiner. IB is the first stage of utilization behavior (UB). Neuropsychological examination of 40 patients with IB, of 35 with UB, and of 50 disease controls demonstrates the existence of a frontal syndrome and two determining features of such behavior: dependence on (1) the social and (2) the physical environments. Loss of intellectual control was also required for the occurrence of such behavior. UB and/or IB were present in 96% of the 29 patients with focal lesions of the frontal lobes. Computed tomographic scans in 26 of these patients showed involvement of the inferior half of the anterior part of one or both frontal lobes. IB and UB are interpreted as release of parietal lobe activities, resulting from impairment of frontal lobe inhibition.

Disturbances of verbal memory in local lesions of the left and right cerebral hemispheres.

Views regarding the multichannel character of information coding that have been put forward suggest that different zones of the left (dominant for speech) and right hemispheres make a specific contribution to verbal memory processes. Clinical facts have led to enunciation of the hypothesis that the left hemisphere participates in processing of the characteristics of verbal material at a higher level (semantic) and in the right hemisphere participate in processing of characteristics at a lower level (sensory) [8~ 9]. In the investigation described below the aim was to determine the role of the left and right hemispheres of the human brain in processing of various semantic and sensory characteristics of verbal material under conditions of voluntary memorizing. Altogether 20 patients with local brain lesions were studied: 12 had lesions of the left and eight lesions of the right hemisphere. Patients with lesions in the left hemisphere were divided into three groups: i) patients with variants of the frontal syndrome; 2) patients with variants of the temporal syndrome; 3) patients with variants of the parietal syndrome. Group 4 consisted of patients with lesions of the temporo-parietal zones of the right hemisphere. The location of the lesion was verified from the results of operation or the results of objective tests (angiography, roentgenography, electroencephalography, etc.) The patients were capable of being tested by the techn~aue chosen and they had no marked speech disorders. The control group consisted of !00 healthy subjects~ selected by age and level of education. A modified version of the technique known as '~two groups of words with three words in each group" that is traditionally used for the neuropsychoiogical investigation of memory [i] was used in the experiment. The words in the groups were chosen with allowance for frequency, various semantic, and sensory characteristics. In the experiments of series I the groups contained words similar or identical in meaning (the "semantic field" structure~ for example: "boldness -- valor -- courage"). In series II the words were grouped together in accordance with the principle of situation association, so that they could be combined into a larger semantic unit -- a pattern or sentence (a "situation association" structure~ for example: "thunderstorm-- lane -- puddle)."In series III phonetically similar words were used (the "phonetic similarity" structure~ for example: "Uzor --Upor -- Ukor~')o The choice of

Frontal lobe dysfunctions in schizophrenia—II. impairments of psychological and brain functions

In Part I of this paper (Levin, 1984), it was proposed that the phenomena of eye movement impairments in schizophrenia are consistent with a dysfunction of frontal eye field mechanisms of ocular-motor control. In Part II, a frontal lobe dysfunction in schizophrenia is also proposed on the basis of clinical, psychological, neurochemical, and neuropathological grounds. There are striking similarities between the clinical frontal syndrome and negative symptom schizophrenia. Parallels between experimental studies of disturbances in attention and information processing, in humans and animals with frontal lobe lesions on the one hand, and in schizophrenics on the other, are noteworthy. The evidence for seemingly disparate dysfunctions in schizophrenia of eye movements, psychomotility, cognition, arousal, motivation and affect, is consistent with a disruption of frontal lobe mechanisms of stimulus-response and drive-response modulation. Studies of the neurochemistry and neuroanatomy of schizophrenia provide further evidence for a frontal lobe dysfunction in a subgroup of schizophrenic patients, particularly those with negative symptoms.