Hippocampus in health and disease: An overview

Postictal Mania: A Comparison with Postictal Psychosis. 1 Takuji Nishida, 1 Tatsuya Kudo, 1 Yushi Inoue, 1 Fumihiro Nakamura, 1 Masaki Yoshimura, 1 Hidemoto Kubota, and 1 Tateki Fujiwara ( 1 National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka, Japan ). Purpose: The present study aimed to differentiate clinical features of postictal mania from those of postictal psychosis and investigate the pathogenesis of postictal mania. Patients and Methods: Four patients who manifested a manic state in the postictal period (postictal mania group) were compared with 15 patients who manifested a psychotic state in the postictal period (postictal psychosis group). Mental disorders were diagnosed according to the ICD-10 criteria. Organic and functional abnormalities in the cerebral cortex were detected using magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT). The epileptogenic zone was estimated by clinical seizure manifestations and laboratory findings including interictal electroencephalography (EEG), ictal EEG, magnetoencephalography (MEG), MRI, interictal SPECT, and ictal SPECT. The Mann–Whitney U test was used for statistical analysis of data. Postictal mania group: All four patients were right-handed men. Seven manic episodes that fulfilled the ICD-10 criteria for manic episode (F30) were observed by psychiatrists in our hospital. One patient had a past history of febrile convulsions and one had encephalitis. One patient had a paternal relative with bipolar mood disorder and one had a cousin with febrile convulsions. The mean full-scale intelligence quotient (FSIQ) on Wechsler Adult Intelligence Scale-Revised (WAIS-R) was 84.8 (SD, 16.5; range, 64–104). The patients in the postictal mania group showed euphoric and elated mood, grandiosity, religious delusion, and flight of idea during the postictal period. Postictal psychosis group: Eight patients were men (all right-handed) and seven were women (six were right-handed and one was left-handed). Fifteen psychotic episodes that fulfilled the ICD-10 criteria for acute transient psychotic state (F23) were observed by psychiatrists in our hospital. Four patients had a past history of febrile convulsions, two had febrile convulsive status, two had meningioencephalitis, and one had brain abscess. One patient had a brother with afebrile convulsion, two had a brother with febrile convulsions, and one had a cousin with febrile convulsions. The mean FSIQ on WAIS-R was 70.4 (SD, 17.5; range, 41–101). The patients in the postictal psychosis group showed various kinds of delusions, most frequently persecutory delusions, auditory hallucinations, somatic hallucinations, Capgras symptom, monolog, and lability of mood during the postictal period. Results: Clinical features of epilepsy: The mean age at the onset of epilepsy was 20.3 years (SD, 9.8; range, 15–35 years) in the postictal mania group and 9.9 years (SD, 6.1; range, 3–20 years) in the postictal psychosis group. Two patients in the postictal mania group had simple partial seizures (reminiscence in one patient and motor seizure of the upper limb in another). On the other hand, 11 patients in the postictal psychosis group had simple partial seizures (epigastric sensations in four patients, auditory hallucinations in three patients, fear in one patient, jamais vu in one patient, cephalic sensations in one patient, and discomfort sensations in one patient). Three patients in the postictal mania group had complex partial seizures, and all four had secondarily generalized seizures. All 15 patients in the postictal psychosis group had complex partial seizures and secondarily generalized seizures. Localization of organic and functional abnormalities in cerebral cortex: The organic and functional abnormalities in cerebral cortex were located in the left temporal lobe in one patient and in left temporal and frontal lobes in three patients in the postictal mania group; whereas they were located in the left mesial temporal lobe in four patients, right mesial temporal lobe in two patients, bilateral mesial temporal lobes in two patients, left temporal lobe in three patients, right temporal lobe in one patient, right temporo-parieto-occipital lobe in two patients, and no definite abnormality in one patient in the postictal psychosis group. Epileptogenic zone: In the postictal mania group, the epileptogenic zone was estimated to be in left temporal lobe in one patient and in left frontal lobe in three patients. In the postictal psychosis group, the epileptogenic zone was estimated to be in the left temporal lobe in eight patients and in the right temporal lobe in six patients. Among these 14 patients, the epileptogenic zone was estimated to be in the left mesial temporal lobe in five patients and in the right mesial temporal lobe in one patient. The epileptogenic zone of the remaining patient was presumed to be in the right hemisphere but the localization could not be decided. Epileptic syndromes: Three patients had frontal lobe epilepsy and one patient had temporal lobe epilepsy in the postictal mania group, whereas 14 patients had temporal lobe epilepsy and one patient had symptomatic localization-related epilepsy with an unknown focus in the postictal psychosis group. Among the 14 patients with temporal lobe epilepsy in the postictal psychosis group, six patients had mesial temporal lobe epilepsy. Clinical features of mental disorders: The mean age of the first episode of mental disorder was 30.3 years (SD, 5.9; range, 23–35 years) in the postictal mania group and 28.1 years (SD, 8.2; range, 14–46 years) in the postictal psychosis group. The mean duration from the onset of epilepsy to the first episode of mental disorder was 10.3 years (SD, 7.6; range, 1–19 years) in the postictal mania group and 18.1 years (SD, 7.6; range, 3–31 years) in the postictal psychosis group. The postictal mania group had, on average, 8.5 manic episodes (SD, 5.6; range, 3–16 times) and the postictal psychosis group had, on average, 2.2 psychotic episodes (SD, 4.4; range, 1–18 times). The mean number of mental disorder episodes was significantly larger (p < 0.05) in the postictal mania group, although the mean duration from the first episode of mental disorder to the last follow-up was shorter in the postictal mania group (mean, 6.5 years; SD, 3.9; range, 2–11 years) than that in the postictal psychosis group (mean, 6.7 years; SD, 3.9; range, 1–15 years). Clinical features of postictal episodes of mental disorders: Both the postictal mania group and postictal psychosis group had complex partial seizures and secondarily generalized seizures preceding the postictal episodes. All postictal episodes had a lucid interval before psychiatric symptoms developed, with a mean duration of 1.9 days (SD, 0.6; range, 1–3 days) in the postictal mania group and 2.0 days (SD, 2.3; range, 0.5–9 days) in the postictal psychosis group. The mean duration of the episodes was significantly longer (p < 0.05) in the postictal mania group (mean, 15.3 days; SD, 12.0; range, 5–49 days) than in the postictal psychosis group (mean, 6.4 days; SD, 6.0; range, 2–23 days). Conclusion: Postictal mania can be differentiated from postictal psychosis by psychiatric symptoms. Compared to postictal psychosis, postictal mania tended to develop sooner after the onset of epilepsy. Patients with postictal mania had more recurrent maniac episodes compared to the number of psychotic episodes in patients with postictal psychosis, and the postictal manic episode lasted for a longer period than the postictal psychotic episode. Organic and functional abnormalities in the cerebral cortex suggested that postictal mania was associated with the frontal and temporal lobes and postictal psychosis with the temporal lobe. Postictal mania was related to frontal lobe epilepsy and postictal psychosis was associated with temporal lobe epilepsy, especially mesial temporal lobe epilepsy. Thus, postictal mania and postictal psychosis are considered to have different pathogeneses.

Deoxyribonucleic acid (DNA) integrity plays a significant role in cell function. There are limited studies with regard to the role of DNA damage in bipolar affective disorder (BP). In the present study, we have assessed DNA integrity, conformation, and stability in the brain region of bipolar depression (BD) patients (n=10) compared to age-matched controls (n=8). Genomic DNA was isolated from 10 postmortem BD patients’ brain regions (frontal cortex, Pons, medulla, thalamus, cerebellum, hypothalamus, Parietal, temporal, occipital lobe, and hippocampus) and from the age-matched control subjects. DNA from the frontal cortex, pons, medulla, and thalamus showed significantly higher number of strand breaks in BD (P<0.01) compared to the age-matched controls. However, DNA from the hippocampus region was intact and did not show any strand breaks. The stability studies also indicated that the melting temperature and ethidium bromide binding pattern were altered in the DNA of BD patients’ brain regions, except in the hippocampus. The conformation studies showed B-A or secondary B-DNA conformation (instead of the normal B-DNA) in BD patients’ brain regions, with the exception of the hippocampus. The levels of redox metals such as Copper (Cu) and Iron (Fe) were significantly elevated in the brain regions of the sufferers of BD, while the Zinc (Zn) level was decreased. In the hippocampus, there was no change in the Fe or Cu levels, whereas, the Zn level was elevated. There was a clear correlation between Cu and Fe levels versus strand breaks in the brain regions of the BD. To date, as far as we are aware, this is a new comprehensive database on stability and conformations of DNA in different brain regions of patients affected with BD. The biological significance of these findings is discussed here.

The World Health Organization (WHO) is revising the ICD-10 classification of mental and behavioural disorders, under the leadership of the Department of Mental Health and Substance Abuse and within the framework of the overall revision framework as directed by the World Health Assembly. This article describes WHO's perspective and priorities for mental and behavioural disorders classification in ICD-11, based on the recommendations of the International Advisory Group for the Revision of ICD-10 Mental and Behavioural Disorders. The WHO considers that the classification should be developed in consultation with stakeholders, which include WHO member countries, multidisciplinary health professionals, and users of mental health services and their families. Attention to the cultural framework must be a key element in defining future classification concepts. Uses of the ICD that must be considered include clinical applications, research, teaching and training, health statistics, and public health. The Advisory Group has determined that the current revision represents a particular opportunity to improve the classification's clinical utility, particularly in global primary care settings where there is the greatest opportunity to identify people who need mental health treatment. Based on WHO's mission and constitution, the usefulness of the classification in helping WHO member countries, particularly low- and middle-income countries, to reduce the disease burden associated with mental disorders is among the highest priorities for the revision. This article describes the foundation provided by the recommendations of the Advisory Group for the current phase of work.

Mental and neurological disorders and risk of COVID-19 susceptibility, illness severity and mortality: A systematic review, meta-analysis and call for action

Electrical stimulation of the medial temporal lobe (MTL) has the potential to uncover causal circuit mechanisms underlying memory function. However, little is known about how MTL stimulation alters information flow with frontoparietal cortical regions implicated in episodic memory. We used intracranial EEG recordings from humans (14 participants, 10 females) to investigate how MTL stimulation alters directed information flow between MTL and PFC and between MTL and posterior parietal cortex (PPC). Participants performed a verbal episodic memory task during which they were presented with words and asked to recall them after a delay of ∼20 s; 50 Hz stimulation was applied to MTL electrodes on selected trials during memory encoding. Directed information flow was examined using phase transfer entropy. Behaviorally, we observed that MTL stimulation reduced memory recall. MTL stimulation decreased top-down PFC→MTL directed information flow during both memory encoding and subsequent memory recall, revealing aftereffects more than 20 s after end of stimulation. Stimulation suppressed top-down PFC→MTL influences to a greater extent than PPC→MTL. Finally, MTL→PFC information flow on stimulation trials was significantly lower for successful, compared with unsuccessful, memory recall; in contrast, MTL→ventral PPC information flow was higher for successful, compared with unsuccessful, memory recall. Together, these results demonstrate that the effects of MTL stimulation are behaviorally, regionally, and directionally specific, that MTL stimulation selectively impairs directional signaling with PFC, and that causal MTL-ventral PPC circuits support successful memory recall. Findings provide new insights into dynamic casual circuits underling episodic memory and their modulation by MTL stimulation.SIGNIFICANCE STATEMENT The medial temporal lobe (MTL) and its interactions with prefrontal and parietal cortices (PFC and PPC) play a critical role in human memory. Dysfunctional MTL-PFC and MTL-PPC circuits are prominent in psychiatric and neurologic disorders, including Alzheimer's disease and schizophrenia. Brain stimulation has emerged as a potential mechanism for enhancing memory and cognitive functions, but the underlying neurophysiological mechanisms and dynamic causal circuitry underlying bottom-up and top-down signaling involving the MTL are unknown. Here, we use intracranial EEG recordings to investigate the effects of MTL stimulation on causal signaling in key episodic memory circuits linking the MTL with PFC and PPC. Our findings have implications for translational applications aimed at realizing the promise of brain stimulation-based treatment of memory disorders.

This chapter reviews how disturbed sleep and circadian rhythms relate to psychiatric and neurological disorders. Nighttime sleep disturbances, daytime hypersomnia, and disrupted circadian rhythms occur in the majority of people with psychiatric or neurological disorders. Evidence supporting that sleep and brain disorders have a bidirectional relationship, such as sleep disturbances increasing the risk of developing neuropsychiatric disorders and neuropsychiatric disorders disrupting sleep, is reviewed. This chapter also discusses how sleep and circadian rhythms play a key role in cognitive and emotional processes tightly linked to neurological and psychiatric disorders, and that not all forms of sleep and circadian rhythms disruption are equally associated with the different types of psychiatric or neurological disorders. This chapter also reviews how medications used to improve sleep are used to treat psychiatric or neurological disorders, and how therapies used to treat psychiatric or neurological disorders can differentially improve or disrupt sleep.

Hippocampal neuron loss and reactive astrogliosis are pathological features of medial temporal lobe epilepsy. Here, the expression of hippocampal astrogliosis-associated genes are studied in subjects with medial temporal lobe epilepsy and mental disorders (such as depression, anxiety and psychiatric comorbidities). The relationship between functional changes in hippocampus astrocytes and concurrent mental disorders are discussed. Nissl staining identified medial temporal lobe epilepsy-induced neuronal loss in the CA1 region of hippocampus. Quantitative real-time polymerase chain reaction and immunofluorescence technology were used to detect hippocampus glial fibrillary acidic protein, metallothionein, and aquaporin-4. The hippocampus area of subjects with medial temporal lobe epilepsy (with or without mental disorders) were smaller than the control group. Hippocampal neuronal loss and astrogliosis were more obvious in groups of medial temporal lobe epileptic patients with mental disorders. Relative protein levels of glial fibrillary acidic protein, metallothionein-I/II, and aquaporin-4 were significantly higher in subjects with medial temporal lobe epilepsy than seen in controls. Medial temporal lobe epileptic patients with mental disorder or depression had elevated metallothionein-I/II protein level when compared to controls and medial temporal lobe epileptic patients without mental disorder. Protein levels of glial fibrillary acidic protein and aquaporin-4 in medial temporal lobe epileptic patients with mental disorders were significantly lower than that in medial temporal lobe epileptic patients with no mental disorder. It is concluded that functional changes in hippocampus astrocytes are associated with mental disorders in medial temporal lobe epileptic patients and the astrogliosis-related genes of glial fibrillary acidic protein, metallothionein-I/II and aquaporin-4, are involved in this process.

Identifying psychiatric and neurological comorbidities associated with hoarding disorder through network analysis

Persistent Auditory Hallucinations That Are Unresponsive to Antipsychotic Drugs

A. Anatomic Classification 1. Idiotypic primary cortex (sensory or motor, e.g., primaryvisual cortex) a. Initial cortical processing of afferent sensory input orsource of primary motor efferents b. Modality-specific c. Directly connected with association cortices and subcor-tical modulating nuclei (e.g., basal ganglia, thalamus) 2. Homotypic unimodal association cortexa. Usually anatomically close to respective primary cortex; modulates the function of primary cortexb. Modality-specific c. Directly connected not only to respective primary cortexbut also with heteromodal association cortex (convergence of pathways) and subcortical modulating nuclei (e.g., basal ganglia, thalamus)3. Homotypic heteromodal (multimodal) association cortex a. Directly connected with each other and unimodal associ-ation cortices (including the limbic and paralimbic regions)b. Two major areas 1) Anterior heteromodal association area (prefrontal cor-tex): concerned with planning of movements and executive functions2) Posterior heteromodal association area (parietotemporalareas, junction between parietal, temporal, and occipital lobes): visuospatial perception and language4. Limbic and paralimbic cortex a. Corticoid areas: basal forebrain (primitive organizationwithout discernable lamination in some areas; least differentiated) 1) Amygdala complex 2) Septal nuclei 3) Substantia innominata (basal nucleus of Meynert)b. Allocortex 1) Hippocampal complex and piriform or primaryolfactory cortex (paleocortex) 2) One or two bands of neurons arranged in externaland internal pyramidal layers c. Mesocortex (paralimbic structures)1) Parahippocampal region 2) Orbitofrontal cortex 3) Temporal pole 4) Insula 5) Cingulate cortexB. Histology 1. Cell typesa. Pyramidal cells 1) Pyramidal-shaped cells with apical dendrites extendingtoward cortical surface 2) "Projection neurons" involved in transmitting signalsto other cortical, subcortical, or spinal areas 3) Located mainly in layers III, V, and VI 4) The neurotransmitter is glutamate (excitatory)b. Stellate cells 1) Star-shaped neurons with dendritic extensions in alldirections 2) Found in all layers, but most common in layer IV 3) Are local inhibitory interneurons; use γ-aminobutyricacid (GABA) c. Fusiform cells1) Found primarily in layer VIPrimary cortices do not communicate directly with each otherHeteromodal areas are responsible for integration of cortical processes and input from unimodal association areas, which in turn receive input from primary cortices2) Long dendritic processes extend toward cortical surface3) Axons project primarily to thalamus 2. Horizontal cortical organizationa. Neocortex (primary, unimodal, and heteromodal areas) is organized in six layers 1) Layers I to IV receive afferents 2) Layer V projects to spinal cord, brainstem, and basalganglia 3) Layer VI projects to thalamus 4) Corticocortical connections: mainly from layers IIand III of primary cortices to layers V and VI of association corticesb. Layer I-molecular (plexiform) layer: consists mainly of local interneurons and apical dendrites of pyramidal cells in deeper layerc. Layer II-external granular layer 1) Stellate cells: axons project to deeper cortical layers 2) Pyramidal cells: axons project to contralateral cortexas commissural fibers d. Layer III-external pyramidal layer: pyramidal cellswith projections to ipsilateral cortices (association fibers) or contralateral hemisphere (commissural fibers)e. Layer IV-internal granular layer 1) Consists mainly of stellate cells 2) Receives afferent glutaminergic input from thalamus 3) Prominent layer in primary sensory corticesf. Layer V-internal pyramidal layer 1) Pyramidal cells: axons project to basal ganglia, brain-stem, spinal cord, and contralateral cortex (commissural fibers)2) Prominent layer in primary motor cortex, which contains giant pyramidal cells of Betzg. Layer VI-multiform layer: pyramidal cells with projections to thalamus and layer IV3. Vertical (columnar) cortical organization a. Each column is a functional unit of cortex b. Specificity of connection with target cells is maintainedand afferent feedback from the same target is received c. Layer IV is the main input layer in each column d. Afferents from a specific group of neurons in thalamusproject to a designated cortical column (layer IV): the organizational specificity of neuronal columns is mirrored in subcortical modulating nuclei (e.g., thalamus, basal ganglia)4. Intercortical connections a. Association fibers: connection between different corticesin same hemisphere 1) U-fibers (short association fibers) 2) Superior longitudinal fasciculus3) Cingulum (part of the Papez circuit) 4) Inferior longitudinal fasciculus 5) Uncinate fasciculusb. Commissural fibers: connection between the two cerebral hemispheres 1) Corpus callosum 2) Anterior commissure 3) Posterior commissure 4) Hippocampal commissurec. Projection fibers: corticosubcortical fibersC. Cortical Localization 1. Frontal lobea. Primary motor cortex (Brodmann area 4, M I) 1) Type: idiotypic primary cortex 2) Voluntary discrete movements involving direct projec-tions to spinal cord anterior horn cells and subsequent direct activation of a motor unit3) Lesion: contralateral pattern of upper motor neuron weakness a) Acute lesion: hypotonic and flaccid b) Chronic lesion: spastic, increased reflexes4) Stimulation or epileptic activity: partial motor seizures with spread (jacksonian march) reflect somatotopic organization of the areab. Premotor areas (area 6, M II) 1) Type: homotypic unimodal cortex 2) All areas project to primary motor cortex and spinalcord 3) All receive projections from parietal cortex: parieto-premotor pathways are important in goal-directed movements (reaching and grasping)4) Divisions a) Ventral and dorsolateral premotor cortexi) Located on lateral aspect of frontal lobe anterior to M Iii) Input from parietal lobe and medial premotor areasiii) Responsible for initiating motor plans in response to sensory stimuli (e.g., stopping at a red light)iv) Involved in learning to associate a particular sensory stimulus with a particular motor movement (associative learning)b) Supplementary motor cortex (medial premotor area, area 6, M II) i) Located on medial aspect of frontal lobe anteriorto M I ii) Input from ipsilateral parietal lobe and pre-frontal "presupplementary area" iii) Presupplementary area is responsible for learningsequences of a motor plan and supplementary motor cortex is responsible for producing the motor sequence already learned-does not initiate motor plans in response to sensory stimuli as the lateral premotor regions doiv) Blood flow to supplementary motor cortex increases when one is thinking about or planning a movementv) Contains complete bilateral somatotopic representation of the bodyvi) Responsible for coordinating and advance planning of movements on the two sides of the bodyvii) Stimulation/epileptic activity: tonic abduction and external rotation/elevation of the contralateral arm with forced head turn toward elevated arm (fencing posture)c. Frontal eye fields (homotypic unimodal cortex): voluntary conjugate horizontal eye movements (lesion: transient paralysis of contralateral gaze)d. Broca's area 1) Receives connections from Wernicke's area via arcuatefasciculus 2) Projects to premotor areas involved in motor programsrequired for speech production 3) Lesion: nonfluent aphasia, typically involving deficitsin both language production and motor speech outputs 2. Prefrontal lobea. Type: homotypic heteromodal cortex (all three regions discussed below)b. Dorsolateral prefrontal cortex 1) Located on convexity of the gyri anterior to areas 8and 45 2) Interconnects with other heteromodal regions, basalganglia, and dorsomedial thalamus 3) Important for executive functions, planning, judgment,problem-solving 4) Lesion: poor abstract thought, poor planning, poorjudgment and problem solving, psychomotor retardation, motor impersistance and perseveration, poor executive functioning, and dysexecutive syndromec. Orbitofrontal cortex 1) Located on inferior surface of frontal lobes andincludes the frontal poles 2) Widespread interconnection with limbic system andbasal ganglia 3) Responsible for emotional and visceral activities,social behavior, and inhibition of inappropriate behavior in a particular social context as well as judgment4) Responsible for conscious perception of smell:receives input from piriform cortex via thalamic relay 5) Impairment: disinhibited, impulsive behavior; poorjudgment and insight; emotional lability; euphoria and excessive and inappropriate laughter and jocular affect, especially with right hemispheric lesions; speech apraxia; environmental dependency syndrome with utilization; perseveration; hyperorality; hypersexuality6) Impairment also associated with obsessive-compulsive behavior7) Lesions of orbitofrontal cortex a) Meningioma: commonly involving the sphenoidwing or olfactory groove b) Closed head injury: usually affecting orbitofrontaland anterior temporal areas because of the irregular surface of the anterior and middle cranial fossae8) Stimulation/epileptic activity a) Motor and gestural automatisms that may be com-plex (bicycling, walking around the room) b) Olfactory hallucinations and forced thinking withanterior frontopolar focus d. Mesial frontal cortex and anterior cingulate cortex1) Interconnections with limbic system (especially amygdala)2) Important role in initiation, motivation, and goaloriented behavior3) Impairment: abulia, indifference, poor speech output, impaired initiation of a behavior or motor movement with reduced spontaneous movements; associated with urinary incontinence and gait disturbance4) With severe impairment: akinetic mutism (no spontaneous behavior)5) Anterior cerebral artery distribution strokes orruptured anterior communicating artery aneurysms can selectively involve mesial frontal structures6) Stimulation/epileptic activity: complex motor and gestural automatismse. Wisconsin Card Sorting Test 1) Sensitive measure of function of prefrontal cortex 2) The subject is asked to sort the cards according to acertain perceptual attribute of a visual stimulus (e.g., color, form, number) and, then, challenges the subject to shift cognitive sets without warning3) Patients with frontal lobe lesions have difficulty with this task because of poor cognitive flexibility and perseveration)3. Parietal lobe a. Primary somatosensory cortex (S I, postcentral gyrus):idiotypic primary cortex b. Secondary somatosensory cortex (S II) on the parietaloperculum (on superior lip of sylvian fissure): homotypic unimodal cortex 1) Direct input from thalamus and postcentral gyrus(S I) 2) Bilateral receptive fields (mostly contralateral),receives and integrates information from both sides of the body3) Provides somatosensory input to motor cortex 4) Projections to limbic system: important for tactilelearning c. Dorsal M pathway: occipitoparietal visuospatial pathwayresponsible for visuomotor tasks (see below) d. Impairment1) Lesion of primary somatosensory cortex (S I): primary somatosensory deficits (e.g., touch, vibration, joint position, stimulus localization), sparing pain and temperature sensations, which are projected to second somatosensory cortex (S II)2) Lesion of S II at parietal operculum: pseudothalamic syndrome a) Impairment of pain and temperature (may havecomplete loss of elementary sensory modalities) b) Syndrome of delayed pain and paresthesias, as mayoccur sometimes with thalamic infarcts 3) Parietal somatosensory association corticesa) Complex somatosensory functions b) Lesions produce "cortical sensory deficits" (e.g.,two-point discrimination, graphesthesia, stereognosis, and recognition of bilateral simultaneous stimulation)4) Impairment of nondominant hemisphere: anosognosia, dressing apraxia, geographic agnosia, constructional apraxia, hemispatial sensory neglectLesions of Prefrontal Cortex Dorsolateral: poor executive functions, planning, judgment, and problem solvingOrbitofrontal: disinhibition, impulsive behavior, poor judgment and insightMedial frontal and anterior cingulate Abulia, indifference, poor speech output, impaired initiation of a behavior or motor movement with reduced spontaneous movementsAssociated with urinary incontinence and gait disturbance5) Lesions of dominant hemisphere: finger agnosia, acalculia, agraphia, alexia, aphasia (primarily conduction aphasia and/or transcortical sensory aphasia), right-left disorientation, conduction apraxia a) Angular gyrus syndrome (lesion of angular gyrus,heteromodal cortex): anomia, alexia, constructional difficulties, acalculia, dysgraphia, finger anomia, right-left disorientation (aphasia may be present if lesion extends to superior temporal gyrus and Wernicke's area)b) Gerstmann's syndrome: acalculia, dysgraphia, finger anomia, right-left disorientation6) Lower homonymous quadrantanopia from damage to optic radiations (if lesion extends deep enough)7) Balint's syndrome: optic ataxia, ocular apraxia, simultanagnosia (bilateral lesions)8) Reduced slow phase of optokinetic nystagmus 4. Temporal lobea. Primary auditory cortex (idiotypic primary cortex) 1) Located on dorsomedial aspect of superior temporalgyrus 2) Has a well-defined tonotopic map reflecting cochlearorganization 3) Unilateral lesions do not cause hearing loss, butsubject may have difficulty localizing sound stimuli in space, especially from the opposite sideb. Auditory association cortex (homotypic unimodal cortex): no well-defined tonotopic mapc. Wernicke's area d. Middle and inferior temporal lobes: memory and learning e. Limbic area: inferior and medial temporal areas f. Uncus receives olfactory and gustatory input g. Subcortical occipitotemporal projections and opticradiations (Meyer's loop) h. Insular cortex: taste area II (taste area I is on dorsal aspectof lateral sulcus near insular cortex) i. Impairment1) Superior homonymous quadrantanopia 2) Cortical hearing loss with bilateral temporal (or sub-cortical) lesions 3) Auditory agnosia with lesions of bilateral, more thanunilateral, temporal cortex (and/or corresponding subcortical areas): difficulty recognizing different sounds (nonverbal auditory agnosias may also result from right-sided lesions)4) Dysacusis: perception of particular sounds as unpleasant5) Pure word deafness (often bilateral lesions) a) A verbal auditory agnosia (due to auditory-verbaldisconnection)b) Patients can hear and react to environmental auditory cues and can understand written language, but are unable to understand spoken language6) Wernicke's aphasia (dominant lesions) 7) Klüver-Bucy syndrome: bilateral anterior temporallobe lesions (see below) 8) Amnesiaa) Nondominant hemisphere: amnesia for nonverbal, visuospatial informationb) Dominant hemisphere: amnesia for verbal information)9) Amusia a) Example of nonverbal auditory agnosia b) Difficulty with recognition of songs, primarilybecause of disturbance of recognition of different characteristics of music composition (e.g., rhythm, pitch, tone) due to right temporal lobe lesionsc) Left temporal lobe lesions: not true amusia, patient has difficulty understanding lyricsd) Left temporal lobe lesions in musicians who analyze different aspects of music composition may produce some degree of amusia10) Ageusia (lack of taste): possibly occurs with bilateral lesions of insular cortex11) Semantic dementia: dominant anterior temporal lobe is site of word meaning (object-word associations)12) Prosopagnosia (defined below) a) Lesion in posteroinferior temporo-occipital region b) Usually bilateral lesions, but nondominant hemi-sphere lesion may be sufficient j. Stimulation/epileptic phenomena1) Complex visual hallucinations of people, animals, etc. from a posterior temporal lobe epileptic focus2) Auditory hallucinations 3) Olfactory hallucinations (especially unpleasant odor,"uncinate fits"), gustatory hallucinations, epigastric rising sensation, intense fear (or pleasure), usually associated with alteration of consciousness and associated with complex partial seizures arising from medial temporal lobe4) Alternation of memory a) Déjà vu: sensation of familiarity with a previouslyunfamiliar experience, place, or event b) Déjà entendu: sensation of familiarity with apreviously unfamiliar auditory experience (e.g., sound, music, speech, or narrative)c) Jamais vu: sensation of unfamiliarity with a previously familiar experience, place, or eventd) Jamais entendu: sensation of unfamiliarity with a previously familiar auditory experiencesymptoms such as amaurosis, scotoma, or visual field defects)b) Eye deviation, nystagmoid eye movements5) Palinopsia a) Recurrence of an image no longer present in visualfield b) May occur with posterior temporo-occipitalepileptic focus 6) Automatisms are associated with the complex partialseizures arising from, or spreading to, mesial temporal lobe7) Postictal cough 5. Occipital lobea. Primary visual (striate) cortex (V1) 1) Type: idiotypic primary cortex (area 17) 2) Located along the banks of calcarine fissure 3) Layer IVa) Receives the majority of input from lateral geniculate nucleusb) Projects primarily to layers II and III, which then project to association cortices4) Projections to superficial layer of superior colliculus and pulvinar: responsible for production of saccades and rapid shifting of gaze to another point in the visual field in response to a novel stimulus a) Other sensory cortices project to deep layers ofsuperior colliculus b) Superior colliculus acts as a sensory integration center c) Novel visual stimulii) Retinal ganglion cells and primary visual cortex project to superior colliculus (e.g., moving vehicle entering the far right visual field)ii) Other sensory input (e.g., auditory-projections from corresponding primary sensory [auditory] cortex) to deep layers of superior colliculusiii) Superior colliculus: integrated sensory response to direct gaze toward novel stimuli5) Occipital pole: central (macular) vision 6) More anterior portions of calcarine cortex: peripheralvision 7) Impairmenta) Homonymous hemianopsia: may or may not spare macular area (vascular lesions often spare the macula because of dual blood supply)b) Anton's syndrome: bilateral lesions of medial occipital lobe (usually acute onset) cause cortical blindness associated with denial of the deficit, of which the patient is unaware, and confabulation8) Stimulation/epileptic phenomena a) Simple elementary visual hallucinations, primarilygeometric shapes and (usually but may be Cortical Angular gyrus angular gyrus lesion alexia, constructional difficulties, acalculia, dysgraphia, finger anomia, right-left disorientation syndrome Dominant angular gyrus lesion dysgraphia, finger anomia, right-left syndrome Bilateral medial occipital lobe lesion Cortical blindness associated with denial of the deficit, for which the patient is unaware, and syndrome Lesion occipitotemporal pathways often with ataxia, ocular apraxia, simultanagnosia Klüver-Bucy anterior temporal lobe lesion and behavior, emotional of response to fear and and activity syndrome that the are the patient as in context of that a is an Usually associated with in the context of syndrome of are but not in context of and but may also be in syndrome to produce an internal image of a the to inferior temporal primarily with perception of and important in recognition of and and pattern cells do to in Impairment of can cause i) visual visual or the the lesions usually involve occipital or bilateral occipitotemporal this is in to visual agnosia in which perception is and patient can the but is unable to the disturbance may be in lesions involving the posterior parietal area, sparing the cortices responsible for cortical blindness with lesions of inferior association areas 1) Type: homotypic unimodal cortex 2) Located in the occipital areas and middle and inferior temporal gyri of visual input perception of different aspects of visual input as well as perception of and integration with other sensory projections to parietal and temporal Dorsal M a) in M cells of that project to of lateral geniculate nucleus b) dorsal to middle temporal medial superior temporal areas to the posterior parietal area i) and in the in is primarily the junction of parietal, and temporal Bilateral lesions of can cause agnosia to M cells do not to in but neurons are to primarily in the M information on perception of of and of a particular visual Important for and information about the of an in optic and Important role in shifting of gaze in response to visual ocular Important for understanding the meaning of an image as a in simultanagnosia perception of different of the Balint's syndrome: the of optic ataxia, ocular apraxia, and simultanagnosia (usually occurs with bilateral Other of impairment: or bilateral inferior slow of optokinetic Ventral a) in cells in that project to of lateral geniculate in the hemisphere or and a superior quadrantanopia because the lesion inferior cortex to the calcarine or inferior temporal patient can but of (e.g., patient that the of is difficulty recognizing familiar and lesion occipitotemporal areas or affecting Difficulty the characteristics and of and Unilateral or bilateral superior and of and the of 1. complex of most organization is in and have dendrites to Receives input from major and sensory cerebral cortex, for of Projects to cerebral cortex directly or via thalamic relay to cortical Interconnections between thalamus and cerebral are important for coordinating cortical activity and processing sensory most important for 1) Projections to basal forebrain and for 2) Lesion may cause functional 1) to thalamic nucleus inhibitory projections to other thalamic 2) to and basal forebrain 3) cortical mainly from and h. 2) receives afferent 3) responsible for 1) forebrain important in of behavior, projections to thalamus and important in of and neurons a) Located in nuclei of b) Reduced with from to 3) Located in and b) group is in c) Responsible for of Cortical of the occipital lobe inferior to the calcarine involving the inferior occipitotemporal produce a superior visual field and loss of vision in the inferior visual field perception of both the superior and inferior visual fields are but the superior visual field the of the superior Patients to and is more when are in a particular of a (e.g., is of and familiar to the patient is and may use other such as or a to the difficulty and emotional to the right gyrus more to gyri Responsible for of which modulates and of in response to of stimuli i) activation for ii) activation associated and increased emotional 4) a. connections with b. local inhibitory projections to thalamic nuclei nucleus and nuclei b. neurons project to cerebral cortex: of 1. Inferior posterior parietal cortex and the primary sensory cortices are important for perception of a novel stimulus and initiation of a response to the stimulus a. Superior and parietal lobe connections with the frontal eye all important for perception of a novel visual cortices selectively the thalamic nucleus and the inhibitory of this nucleus on other thalamic thalamic relay of sensory Prefrontal cortex (especially mesial frontal frontal eye and anterior cingulate cortex are responsible for and selectively on the novel stimulus to the important stimuli in the as well as a. Lesion can cause motor perseveration, and akinetic mutism with severe of the mesial frontal lobes or a cortical (especially a. Projects to prefrontal areas and is an important prefrontal function b. Lesion of or or 4. Primary and association sensory cortices 5. and and are important in of of 1. Acute b. Chronic of and memory as a (e.g., c. or other d. Subcortical associated and possibly other frontal lobe may be of projections and other subcortical pathways as in or dominant with subcortical infarcts and Unilateral a. Unilateral sensory is with bilateral simultaneous of the of the of the is as of the May be to when is severe of the primary sensory 1) may be to has a 2) the patient the to hemispatial from of the of hemispheric lesions usually cause contralateral usually with hemispheric lesions) 1) hemisphere the inferior parietal for for both sides of the and hemisphere only for the right of the patient is of the deficits (e.g., and perceptual and cognitive most commonly with right hemisphere patient is to the recognition of or often with right hemisphere hemisphere lesions may also be associated with the a) reduced of emotional in speech hemisphere especially right of or disorientation, impaired and in the of right posterior cortex of or right parietal or motor of motor behavior to the primarily a result of sensory and 1. of and experience and alteration of behavior as a result of the form, in response to to the same and for a. behavior can be with of neuronal pathways b. in neuronal and are of and are responsible for learning and or learning of information 5. of previously as memory of memory 1) that conscious and is which is and meaning of people, and and conscious (e.g., for of perception of sensory association cortices and e.g., visual association cortices are involved in and of specific aspects of a particular visual stimulus is of is mesial temporal lobe and and cortices the of of involving association cortices mesial temporal aspects of a particular experience are in different regions, and memory for a experience is in a of a particular region loss of previously in that region and loss of to in that of a) of and abstract to (e.g., Semantic memory association areas and other regions mesial temporal Semantic memory loss usually memory memory loss may be in a of and can also be in in with memory and other i) of that have and with in particular and of that conscious and and conscious memory that not conscious is memory nonverbal Long or more to and cerebral for that occur a event memory loss to to information a particular previously memory 1) that not conscious is slow 2) of memory i) for a motor task the same is slow and the is to Motor learning occurs with the of the and motor and cortical Cortical pathways important for motor motor cortex, premotor cortex, supplementary motor cortex, the parietal lobe (lesion of pathways may produce perceptual is to of memory on the of a. in hemisphere (dominant amnesia for verbal memory of verbal may be with temporal lobe 1) in right hemisphere 2) amnesia for visual memory may be right temporal lobe patient may have difficulty recognizing etc.

BackgroundPrevalence among adolescents with mental disorders are about 20% worldwide. In 2012, Ghana enacted the Mental Health Act, Act 846 to regulate mental health care, but did not include specific programmatic details of service provision nor any measurable indicators for adolescent mental health. Currently no service programmes focused on adolescents and no aggregated data exists documenting prevalence of mental and neurological disorders among adolescents. In the Brong Ahafo region, mental health providers carry out simultaneous programmes to diagnose, treat, and counsel patients. There is a need to investigate how these service programmes are currently functioning as measured by World Health Organisation guidelines. This study therefore, investigated quality of service provision for adolescents with mental disorders in Kintampo North and South districts of central Ghana.MethodsMixed method approach of quantitative and qualitative data collection, organization, and analysis was implored. Quantitative method data collection used case registers to identify mental and neurological disorders among adolescents. Qualitative methods used in-depth interviews of service providers, primary caregivers, and users of healthcare on the services available to treat mental and neurological disorders among adolescents. A combination of quality standards tools was used to assess services.ResultsEpilepsy was the most common treated disorder among adolescents receiving services at the four facilities in the two districts. Providers and stakeholders had limited or no training in adolescent mental health. Validated diagnostic tools were not being used to rule out differential diagnosis; medication procurement was a challenge to consistent treatment. Data collection and analysis was not standardized. Providers, stakeholders, patients, and their primary caregivers reported challenges with funding, transportation logistics, and stigma against people with mental and neurological disorders.ConclusionThere are few mental health service providers for people living with mental disorders in the two Kintampo districts, with no specific services for adolescents. The Mental Health Act 846 of 2012 is an important milestone in mental health care but there are not specific plans for its implementation. Community sensitization, education in mental health and neurological disorders, and advocacy against stigma are all successful programmes that have the potential to be scaled up.

Psychiatric disorders are common in many neurological disorders, including epilepsy, migraine, Alzheimer's disease, Parkinson's disease, essential tremor, and stroke. These comorbidities increase disease burden and may complicate the treatment of the combined disorders. Initial studies of the comorbidity of psychiatric and neurological disorders were cross-sectional, and time order of the associations was impossible to elucidate. More recent work has clarified time associations between psychiatric disorders and neurological disorders, particularly in epilepsy and stroke where epidemiological evidence suggests that there is a bidirectional relationship. This article takes an epidemiological approach to understanding these relationships and focuses mostly on epilepsy. Although, these relationships are understood in many neurological disorders, routine screening for psychiatric disorders in neurological disorders is infrequent, mostly due to the lack of partnerships between psychiatrists and neurologists and the paucity of neuropsychiatrists. Much more needs to be done to improve the detection and treatment of patients affected by neurological and psychiatric disorders. Understanding the scope of this overlap may inspire collaborations to improve the lives of people affected by both disorders.

Lessons From Neuropsychiatry

Toxoplasma gondii (T. gondii) is a globally prevalent intracellular parasite capable of causing latent infections in humans. T. gondii, a widely prevalent protozoan parasite, has been increasingly linked to mental, psychiatric, and neurological disorders. Understanding its seroprevalence is critical to assess its potential public health impact and guide preventive strategies. Despite the extensive research conducted in Türkiye on this association, the outcomes have shown variability. A comprehensive synthesis is required to elucidate the seroprevalence of T. gondii among affected patient groups and to enhance our understanding of the potential public health implications. This study posits that the prevalence of T. gondii among patients with psychiatric and neurological disorders in Türkiye is substantial, with notable socioeconomic and geographical variations. It aims to estimate the seroprevalence of T. gondii infection among these patients in Turkey, adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A systematic review and meta-analysis were performed following the guidelines of the PRISMA. In November 2024, comprehensive searches were conducted across PubMed, Web of Science, Scopus, and the TR index using a set of predetermined keywords without imposing any temporal limitations. The methodological quality of the studies included in the review was evaluated using the Joanna Briggs Institute's Critical Appraisal Checklist, which is applicable to both randomized controlled trials and cross-sectional studies. Data were synthesized using a meta-analytic technique. Prevalence was calculated using a random-effects model with a 95% confidence interval (CI). Cochran's Q and I2 statistics were performed to assess heterogeneity among the included studies, while funnel plots and Egger's tests were used to evaluate publication bias. The prevalence of toxoplasmosis was 34% (95% CI: 28%-39%). When the patient groups of the studies included in the research were classified, the subgroup analysis performed with the obtained data was found to be 34% (95% CI: 28%-39%) in patients with both neurological and psychiatric disorders. This meta-analysis identified a significant seroprevalence of T. gondii infection among individuals with psychiatric and neurological disorders in Türkiye. These findings indicate a potential association between T. gondii exposure and neuropsychiatric conditions, highlighting the need for further research and increased clinical awareness in at-risk populations.

Objective: The purpose of this study is to evaluate the potential diagnostic benefit of SPM-based semi-quantitative FDG-PET analysis in autoimmune encephalitis (AE) compared with visual analysis by experienced neuroradiologists using a larger sample size.Methods: This observational retrospective case series study was conducted from a tertiary epilepsy center between May 2014 and March 2017. Healthy individuals without any neurologic or psychiatric diseases were recruited as control. We determined brain FDG-PET abnormal glucose metabolism on medial temporal lobe and basal ganglia using semi-quantitative analysis and compared this method with visual analysis at the same time among patients with autoantibody positive AE.Results: Twenty-eight patients with clinically diagnosed AE and 53 healthy individuals without any neurologic or psychiatric diseases were recruited. On the medial temporal lobe and the basal ganglia, semi-quantitative analysis showed consistency with the visual assessment for whom they had abnormal metabolism by visual assessment. More importantly, 56% patients on medial temporal lobe and 73% patients on the basal ganglia respectively who were not identified by visual inspection can be detected by semi-quantitative analysis, demonstrating the greater sensitivity of semi-quantitative analysis compared with visual assessment.Significance: This study showed semi-quantitative brain FDG-PET analysis was better than visual analysis in view of observing the abnormal glucose metabolism of patients with autoantibody positive AE. Semi-quantitative FDG-PET analysis appears to be a helpful tool in early diagnosis of patients with AE.