Mental disorders in epilepsy
.pdfIntermediate position in the same type of parameters occupies the type of the course of disease with the set aside exacerbation of process, which is distinctly expressed in the third decade of life.
The traced by us versions of the dynamics of paroxysmal disorders with epilepsy, changes in the personality dependent on age, which do not reach the degree of dementia, psychosis and dementia attest to the fact that to the unfavorable development of disease correspond appearance within a comparatively short period, almost simultaneously, at the earliest stages of the ontogenesis of personal changes, the signs of psychosis and signs of dementia. With the mixed rate of the formation of negative psychopathological syndromes (at first slow, then subacute) the sequential appearance of changes of the personality and psychotic disorders in the age from 20 to 50 years can indicate the possibility of the set aside exacerbation of process, which does not lead, however, to the development of total dementia. Dementia is here more frequently characterized by the predominance of the disorders of thinking in the form the retarding its rate, perseveration, diffusion, ornateness.
The stages of the development of psychopathological disorders isolated by us indicate the possibility of their examination as the basic sections of pathokinesis with the epileptic disease. For the period of inspection the first stage of the development of psychopathological disorders (psychoses) reliably more frequently occurred in patients with the favorable course of epilepsy, the second and third stages (respectively the first and second stages of shaping of dementia) – in the cases of the course of disease with the set aside exacerbation of process, the third and fourth stages (respectively the second and third stages of shaping of dementia) – in patients with the unfavorable course of epilepsy.
The regularities (the so-called averaged model of the types of the course of disease) revealed by us makes possible to assert that the factor dependent on age takes essential part in shaping of clinical picture with epilepsy, which takes place with mental disorders.
Interesting in this respect is the data of study S. Ehlers et al. (1997) about the state of motor activity, speech and the behavior in 303 children from Lennox-Gastaut syndrome in the age classes to 3, from 3 to 8 and older than 8 years. In children at the age of up to 3 years the authors observed delay in the development of motor and vocal spheres. In children at the age from 3 to 8 years vocal disorders prevailed almost in all cases. In the children of older than 8 years predominated social and behavioral problems.
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According to our data, between the floor of patients and the types of the course of disease are absent statistically reliable connections.
To a certain degree this is confirmed by the data about the absence of sexual differences according to the results of the study, carried out by E. Sarac et al. (1997), who studied the fluency of speech in 36 patients with the primarily generalized epileptic seizures.
The results, obtained in the course of clinical and electrophysiological studies, and also the data of the dynamics dependent on age of the isolated by us for the analysis basic syndromes with epilepsy, confirm, therefore, the lawfulness of reference to the basic determinants of the prognosis of the types of the course of epilepsy: favorable type, with the delayed exacerbation and unfavorable type.
Apparently, there is sufficient reason to talk about genetic conditions of the tendency to preserve in every case of the disease mostly of some form of current psychosis: transient, schubweise or chronic. The type of the course of disease as a whole in this case mainly is diagnosed depending on structure and frequencies of the paroxysms, presence in structure of the psychotic syndromes of affective, delusional and catatonic disorders.
To the favorable type of the course of epileptic disease corresponds predominance in patients at the early stages of the ontogenesis of vegetative paroxysms, and also predominance in the structure of the psychosis of the affective disorders in the absence of the signs of epileptic dementia and the presence on the electroencephalogram of indications of localization of epileptic center in “deep” divisions of the brain.
The type of the course of epilepsy with the delayed exacerbation is characterized by the polymorphism of paroxysmal phenomena and by predominance in the structure of the psychosis of delusional and hallucinatory disorders. To it’s characteristic, the presence in the patients of the moderately expressed signs of intellectual-mnestic defect and multi-focus disturbances of the bioelectric activity of the brain.
The unfavorable course of disease develops on the background of cerebral insufficiency. Frequent seizures are polymorphous and generalized in nature. In the structure of polymorphous psychotic states occur catatonic disorders. Early, almost simultaneously with the appearance of psychotic disorders develops epileptic dementia, to the foreground in structure of which comes brutal explosiveness, an inconsistency in the assessment of the surrounding events, torpid, viscosity thinking and mnemonic disorders. The indications of pre-
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dominantly frontotemporal and frontal localization of epileptic focus are frequent on the electroencephalogram.
Prolonged combination in each of the named three basic versions of the course of the disease of the characteristic types of paroxysmal and psychotic disorders can testify the specific localization of pathologic process. Clinical and electrophysiological data are consistent with the prevailing views to date of the existence of trends in preferential epileptization of various functional systems of the brain.
According to N.E. Bharucha et al. (1997), “explanatory models” of the disease in epilepsy provided a clear view of its “local values”. Sh. Bibileishvili (l997) groups the observed by him patients on the prevalence of primary generalized tonic-clonic seizures, secondarily generalized seizures and complex partial seizures. Close to this classification of epilepsy N. Adachi et al. (1997): generalized, temporal and partial, not related to the temporal. N. Holthausen (1997) considers that the use of data about the localization of the underlying epileptic lesions and “modus operandi of seizure”, fit more adequately for the classification of epilepsy than its division into options with simple or complex seizures..
The prevalence of paroxysmal autonomic and affective disorders is apparently an expression of disease syndromes, the original name of which – the limbic epilepsy – was given by PD McLean (1952). The contemporary international classification of epilepsy contains the closest to this concept term mediobasal limbic seizures (G.S. Burd, 1995).
In recent years, more and more often in literature is used the term Mesial Temporal Lobe Epilepsy (D. Cavalcanti et al., 1997; O. Dogu et al., 1997; Y. Kim et al., 1997; K. Lernertz et al., 1997; Y. Mayanagi et al., 1997, and others). In the majority of patients with this diagnosis the authors note partial seizures, partly with motor automatisms and “cognitive activity”. E. Kozima et al. (2011) indicate the special interest in these cases of such divisions of temporal lobe as amygdala, the hippocampus, paralimbic zones and parahyppocampal circumvolution.
The combination of the vegetative, affective, psycho-motor, psy- cho-sensory and generalized convulsive forms of paroxysms with the psychotic disorders of the hallucinatory-delusional content established by us corresponds to data by H. Landolt (1960) and I.S. Tets (1977) about the polymorphism of clinical manifestations with socalled temporal epilepsy.
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E.J. Clarke et al. (1997) note the combination of complex partial seizures with the nonaffective psychoses, listed in DSM-VI-R with temporal epilepsy. S. Field et al. (1997) is described patients with temporal epilepsy less fluent, than in the control, speech, and eventually more verbose and repetitive. N. Holthausen (1997) defines children’s temporal epilepsy as referring to the risk of the appearance of psychiatric problems. Jokeit N. et al. (1997) believe that the risk of “prefrontal metabolic asymmetry” associated with cognitive impairment, increased in patients with left temporal lobe epilepsy of generalized seizures. Macovei M. et al. (1997) provide two cases of familial temporal lobe epilepsy with impaired irritation, localized in the anterior temporal areas, and impaired memory and behavior. In his patients “with the temporal focus” R. Manchanda et al. (1997) observed “the experience of the experience of sensations” and “viscerosensory auras”, whereas “somatosensory and elementary visual auras” more frequently occurred with the nontemporal focus. Thus the patient with auras of “the experience of the experience of sensations” were more likely to experience “psychiatric” disorders. Indications for the surgical treatment of patients with intractable temporal lobe epilepsy P. Moran et al. (1997) counted the extended and varied in them mental disorders and “psycho-social incapacity”. B.K. Toone et al. (1997) note tendency toward the decrease “hippocampal volume” to the left in patients with “chronic interparoxysmal shizophrenia-like epileptic psychoses”.
Noted by us predominance in the clinical picture of the disease of the generalizув convulsive seizures with the frequent states of decompensation and diverse catatonic disorders are present, and also noted by A.R. Luriya (1973) in patients with a neuropsychological study “apraxia target action” evidence in favor of a primary lesion of the frontal lobes.
Frontal or frontotemporal origin of epileptic seizures M. Derouaux et al. (1997) considered frequent in the adult patients with epilepsy patients with severe or profound mental retardation. Sharp psychoses and series of seizures were noted by A.J.C. Russell et al. (1997) in patient with the independent right and left-side frontotemporal foci on interparoxysmal EEG. V. Swartz et al. (1997) by their studies confirm the presence in patients with frontal epilepsy the damages of working storage.
As for the general pathogenetic explanation of syndromogenesis and syndromokinesis paroxysmal and psychotic disorders, the most adequate, in our view, is actively developed in recent years the con-
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cept of formation in the course of the illness of reciprocal relationship between pathologic and normal functional systems of brain (G.N. Kryzhanovskiy, 1981).
In this respect it is appropriate to cite the following data.
In the opinion of V.A. Karlov (2010), there are mechanisms, capable of preventing the propagation of epileptic activity from the focus. First of all it is the base functional state of the brain. It was established in 1970-1980 that the mechanisms of anti-epileptic protection are activated by most epileptic focus and form the system of anti-epi- leptic protection, so called anti-epileptic system (V.A. Karlov, 1974; G.N. Kryzhanovskiy, 1980; and others) as the set of mechanisms, which impede propagation and generalization of epileptic activity. First of all this collateral inhibition around the focus in the form of perifocal brake shaft, which is directed both directly, and through different sub-cortical formations, which possess inhibiting function (caudate nucleus, the cerebellum, the lateral nucleus of hypothalamus and especially orbit-frontal cortex (V.A. Karlov, S.E Petrenko, 1980; and others).
The activation of these structures occurs under the effect of the corticofugal impulses, and they have inhibiting action on epileptic activity by the means of the inhibitory GABAergic influences, which cause the hyper-polarization of cortical neurons, acting as a negative feedback mechanism.
At the same time a number of structures, which possess inhibiting anti-epileptic influence, are located in the brain stem. This can include GABAergic neurons of the upper upper tubercles colliculus (G.N. Kryzhanovskiy, 1997; M.A. Merrill et al., 2003; F.A. Lado et al., 2003), the posterior hypothalamus , and serotonergic neurons of the dorsal seam and noradrenergic locus coeruleus neurons (D. Gervasoni et al, 2000; F.A. Lado et al., 2008 and others). It is shown that an increase in the GABAergic transmission in the black substance prevents the propagation of discharges from the hypothalamus (J.O. McNamura et al., 1984), and so the role of black substance in the suppression of kindling-epilepsy (L.H. Shi et al., 2007).
As it is known, temporal entities in a state of irritation, may have a deterrent effect on the stem and subcortical structures involved in the formation of generalized paroxysms (A.N. Chibisova, 1984). In contrast, the mechanism of formation of emotional behavior in patients with temporal lobe epilepsy cortico-subcortical relationship is particularly important, and the leading role is played
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by subcortical (limbic) link. (B.M. Rachkov, S.L. Yatsuk, 1984). But if we take into consideration that the orbiot-frontal cortex is considered by the majority of researchers as a modulator of cortical activity of the limbic system, then the effects of deep braking of systems or centers (including catatonic stupor) can be explained in the localization of the frontal lobe (G.N. Kryzhanovskiy, 1981; F. Plum and D. Posner, 1986).
Taking into account the existing indications of the migration of epileptic center in the direction to the frontal divisions of the brain (E.L. Gibbs and F.A. Gibbs, 1947, and others) it is possible to assume that the long-standing dynamics of epileptic disease is caused by series connection into the pathologic process of at first mediobasal structures of temporal lobe, and then in the larger volume and with the tendency toward the lateralization – of temporal and as a whole frontal divisions of the brain.
Displacement in the course of the disease of epileptic focus in each individual case, probably, is possible to trace in the direction of the generalization (or “damping”) of the epileptic seizure or of psychotic schub, and also according to the nature of the processes of compensation (G.B. Abramovich, 1964; L.R. Zenkov, 1982). In accordance with the rate of progressive course of disease within the different periods following the more ancient formations into the pathologic process are implicated those superincumbent controlling phylogenetically later formed or “neurologically immature” functional systems of the brain. Less stable than the compensatory mechanisms , the more active epileptic process proceeds.
In its most general form, the results of the mathematical test of this hypothesis point to a trend towards the complexity in the positive symptoms of the disease in cases of initial predominance of mood disorders, as well as the tendency to “regress” of catatonic and delusional syndromes. The first circumstance confirms assumption of “the excursion” process in the direction of the phylogenetically oldest functional systems to more young.
The second circumstance, at first glance seems contradictory to the first, , in clinical terms can be explained taking into account that productive psychopathological symptoms with aggravation of epileptic dementia, as shown by our study, most frequently actually undergoes the reverse development: delusional ideas become less urgent, and catatonic phenomena are reduced, the so-called late remission begins.
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In this light, some hypotheses in recent years are of interest. Occurring at a combination of depression and epilepsy morphological changes shape, in the opinion of A.M. Kanner et al (2002) and Y.I. Sheline (2003), the limbico-cortico-strio-pallido-thalamic circuit, which in turn consists of two branches. The first branch includes amygdala, hippocampus, mesio-dorsal nucleus of thalamus, mesial and ventrolateral prefrontal cortex. The second branch connects with the limbic and cortical regions caudate nucleus, shell and pale sphere. In this context, are also of interest guidelines of YI Sheline et al. (1999) on the efficacy of antidepressants for the prevention of atrophy of the hippocampus. In contrast to patients with schizophrenia, patients with schizophrenia-epileptic psychoses M. Trimble (2009), according to clinical and neuroimaging studies, notes the safety of affective reactions and increase in the dimensions of amygdala.
The studies, directed toward the development of clinico-neuro- morphological correlations with epilepsy, were undertaken in the last 10-15 years. Given unabated debate concerning the alleged existence of a biological relationship and antagonism between epilepsy and schizophrenia, in this chapter it seems appropriate to give a brief overview of the relevant data obtained using the methods of evi- dence-based medicine in the study of epilepsy, including proceeding with mental disorders (0,3-0,4% of population) and schizophrenia (1% of population).
In the opinion of a number of authors (H. Hamad, 1993; I.C. Wright et al, 2000; R.E. Gur et al, 2000; M. Suzuki et al, 2005; N.G. Cascella et al, 2009; S.M. Hartz et al, 2010; P.C. Koolschijn et al, 2010; B.K. Puri, 2010; F. Sundram et al, 2010; F. Irle et al, 2011; A. Prestia et al, 2011) to the general signs of the development of the indicated diseases relate:
●expansion of the ventricles of the brain and the reduction of volumes of the hippocampus and amygdala as evidence of common disorders of the nervous system;
●the role of temporal and other regions of the brain in the development of chronic psychoses;
●significant deficits in gray and white matter of the brain;
●identification of genes that determine complex partial seizures involving auditory function, and genes that determine the rate of progression of structural brain changes in schizophrenia.
According to M.C. Clarke et al (2012), in the persons with the parental history of epilepsy there is twice increased risk of the
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development of psychosis, and in individuals with a parental history of psychosis 2.7 times increased risk of generalized epilepsy. These data is acquired on the study of the population of parents and their children, who were born in Helsinki between the period from 1947 until 1990. General sample composed 9653 families and 23404 human offspring.
With the use of quantitative methods by L. Marsh et al (2001) a comparative MRI study of the group of the patients with temporal lobe epilepsy with the chronic psychosis (n=9), the groups of the patients with temporal lobe epilepsy without the chronic psychosis (n=18) of the group of the patients with schizophrenia (n=46) and the group of healthy (n=57) was conducted. All groups of patients had the expansion of the ventricles of the brain, the decrease of temporal lobe and the decrease of the volume of the gray matter of the brain of frontoparietal region and upper temporal gyrus. Structural anomalies in the group of patients with temporal lobe epilepsy, which takes place with the chronic psychosis, are not limited to temporal portion. The similarity of the revealed scarcities of the gray matter of the brain in this group and in the group of the patients with schizophrenia indicates the presence of predisposition to the chronic psychosis in patients of both groups (table 1).
In our opinion, to the directions of the uses of methods of neuroimaging with diagnostics of epilepsy and schizophrenia can be referred (table 1):
●establishment of localization and the beginning of a paroxysm of epileptic psychosis in resistant (in 30% of cases) to the drug therapy of epilepsy (for resolution of questions of surgical treatment) and the establishment of localization of changes in the volume of the gray and white matters of brain in the period of the demonstration of the first psychotic episode with the schizophrenia;
●the establishment of the connections between the functional systems of the brain: limbic (mesial temporal lobe) and temporalfrontal (upper temporal gyrus and prefrontal cortex);
●the study of the dynamics of changes in the volume (concentration) of the gray and white matters of brain at the different stages of pathologic process with epilepsy and the schizophrenia.
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Table 1
Clinico-neuromorphological correlations with epilepsy and schizophrenia
Localization of the beginning of paroxysm and psychosis
Epilepsy |
Schizophrenia |
|
|
The reduction of the volume of hippo- |
|
campus is located in the close connec- |
|
tion since the beginning of the fit in the |
|
mesial temporal lobe structures |
|
(S.S. Spencer, 1994; J.S. Duncan, 1999) |
|
|
|
With the partial seizures is noted |
|
an increase of the density of benzodi- |
|
azepine receptors in the cortex and the |
|
nuclei of the cerebellum and reduc- |
|
tion in the density in the thalamus |
|
(J.S. Duncan, 1999) |
|
Deviations in the development of the |
|
brain tissue of the very beginning |
|
of disease occur in the frontal, tempo- |
|
ral, parietal and occipital regions of the |
|
cortex of hemispheres, and also in some |
|
subcortical structures of the brain, |
|
including thalamic and caudate nuclei, |
|
in the cerebellum, in truncus of the |
|
brain (R. Kuzmanić-Samija et al, 2008; |
|
B.P. Hermann et al, 2010; E. Hutchin- |
|
son et al, 2010; D.T. Pulsipher et al, |
|
2011; D. Tosun et al, 2011) |
|
|
|
With comparative MRI a study |
With a MRI-study of the be- |
of 58 patients with the diagno- |
ginning of the first psychotic |
sis of temporal lobe epilepsy and |
episode with the schizophrenia |
62 healthy, in patients is noted the to- |
is revealed the reduction of the |
tal reduction in the volume of cerebral |
volume of the gray matter of the |
tissue to 5,8%, white matter – to 9,8%, |
left tail end of the upper temporal |
gray matter – to 3% (with the inter- |
gyrus (Y. Hirayasu et al, 1998), |
est of frontal, temporal, parietal and, |
insular cortex (K. Kasai et al, |
to a lesser degree, the occipital shares |
2003), upper temporal gyrus and |
of the brain) (B. Hermann et al, 2003) |
the right forward section of the |
|
gyrus cingulatus (S. Lui et al, |
|
2009; T. Yoshida et al, 2009) |
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Table 1 (cont.)
Localization of the beginning of paroxysm and psychosis
Epilepsy |
Schizophrenia |
It is not discovered the significant connection between the age of patients at the beginning of interictal psychosis and the type of epilepsy (with the temporal and extratemporal localization of epileptic foci) (N. Adachi et al, 2002)
It is not discovered the significant morphometric differences with temporal lobe epilepsy, which takes place with the psychosis and without the psychosis (N. Rüsch et al, 2004)
There are data about the unfavorable postoperative prognosis in the plan of the beginning of the development
of chronic schizophrenia-like psychosis with temporal lobectomy in the cases of diagnostics of mesial temporal lobe sclerosis and structural disturbances of the amygdala to the operation
(P. Shaw et al, 2004)
The bitemporal lobe disfunction, revealed with a neuropsychological study in combination with video-EEG by monitoring and MRI-study, is the predictor of the appearance of interictal epileptic psychosis (M. Falip et al, 2009)
With MEG a study of the chosen types of spike-dipole patterns is revealed leftside upper-temporalvertical type close coupling with the epileptic psychosis (K. Fukao et al, 2009)
With MRI the study of the anomaly of the volume of hippocampus with the formation of mesial temporal lobe
epilepsy, not connected with pharmacoresistance are frequently double-sided (A.T. Berg et al, 2011)
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