Klüver–Bucy syndrome (KBS) is a neuropsychiatric disorder secondary to temporal lobe damage.
This can be associated with various causes. This syndrome is rarely caused by stroke. We describe the
case of a KBS, admitted to the neurology department of the military hospital of Agadir, in September
2022 secondary to ischemic stroke in middle cerebral artery territory. The patient presented most of the
clinical features of KBS. These neurobehavioral manifestations improved after the start of treatment.

Dear Editor,
Children living with autism spectrum disorder (ClwASD)
face challenges in social interactions and communication
across different settings (classroom, playground,
and home) due to socioemotional challenges.
The Diagnostic and Statistical Manual of Mental
Disorders – 5th Edition mentions deficits in conversations
involving expressive and receptive language for these
children due to abnormal social approaches such as sharing
of reduced interests, affect, pace of communication, social
skill deficits, and emotions.[1]
Lack of facial expressions and poor eye contact
make it nonverbally hard for ClwASD to participate
in communication in social situations. The ability to
integrate body language and gestures with communication
is essentially challenging for most of these children.
Misinterpretation of social cues and language hinders
comprehension of jokes, humors, and metaphors; ClwASD
face challenges in responding to peers and adults by
understanding their emotions and feelings. Many etiologies
are identified for causing ASD, and the spectrum also
encompasses a wide range of intellectual functioning
abilities beyond the neurophysiological changes in the brain.

Autism spectrum disorder (ASD) is an umbrella term
comprising a group of neurological conditions marked by
severe difficulties with social interaction and communication.
According to the World Health Organization,[1] in 100
children worldwide suffer from ASD, and 1 in 500 Indian
children receive an autistic diagnosis. With four men
diagnosed for every female, boys are more likely than
females to be impacted by autism. Compared to Down
syndrome, which affects one in 800 newborns, autism occurs
more often. Children may exhibit a spectrum of symptoms,
varying in intensity, from recurring patterns of limited
interests and unusual behaviors to challenges in transitioning
between activities or events, as well as unexpected reactions
to sensory cues in their surroundings. While a cure for
autism is not currently evident, interventions play a crucial
role in assisting children to effectively manage their
symptoms. By tailoring treatment plans to individual needs,
these interventions contribute to an improved quality of life.

Breastfeeding is the key element of infant feeding and has played a vital role in promoting infant
health throughout history. It provides all the necessary nutrients for infants to grow and develop.
The World Health Organization (WHO) recommends initiating breastfeeding right after birth and
continuing with exclusive breastfeeding for the first 6 months, followed by complementary feeding
up to 24 months of age. The WHO has also set targets to increase exclusive breastfeeding rates by
2025. As scientific research has advanced, the benefits of breastfeeding for infant health have become
increasingly apparent, not only for metabolic diseases but also for cognitive health. As a result,
researchers have started examining whether breastfeeding has any neurological or psychological
effects on lactating mothers. In this review, we examined current research on the neurological and
psychological effects of breastfeeding on women.

Background: Cadmium (Cd) and bisphenol A (BPA) are known industrial additives and
environmental toxicants that have been extensively reported for their various deleterious effects
on biological systems, particularly endocrine disruption and neurotoxicity. In high‑fat diet‑induced
insulin‑resistant model rats, we studied the neurotoxicity and oxidative stress effects of co‑exposure to
Cd and BPA. Aims: This study aims to look at prefrontal microarchitecture and antioxidant profiles in
insulin‑resistant rats. Materials and Methods: Twenty‑five adult Wistar rats were randomly assigned
into five groups (A– E; n = 5). With A receiving normal saline; B: 40 mg/kg. bw CdCl2 + high‑fat
diet (HFD) + Suc; C: 40 mg/kg. bw BPA + HFD + Suc; D: 40 mg/kg. bw BPA + 40 mg/kg. bw
CdCl2 + HFD + Suc; and E: HFD + Suc orally for 56 days. Finally, brains were excised from each
group and the medial prefrontal cortex was dissected from both hemispheres with right hemisphere
samples processed for hematoxylin and eosin histology and left hemisphere samples homogenized
for biochemical evaluation of oxidative stress markers. One‑way analysis of variance and Tukey’s
post hoc test were used for data analysis with P < 0.05 considered statistically significant.
Results: From our findings, prefrontal glutathione levels were significantly lower (P < 0.05) in the
insulin‑resistant rats (Cd + BPA + HFD + Suc: 120.9 ± 21.89, HFD + Suc: 93.27 ± 17.29) compared
with control rats (244.0 ± 11.57), while prefrontal glutathione reductase activity was significantly
elevated (Cd + BPA + HFD + Suc: 41.02 ± 5.5, HFD + Suc: 41.09 ± 1.68, P < 0.05) compared
to the control rats (20.17 ± 3.27). Prefrontal neurons showed nuclear condensation, cytoplasmic
vacuolations, and clumping of cells. Conclusion: Morphological and biochemical evidence from
the present study suggests that environmental and metabolic factors do combine to induce profound
adverse effects on prefrontal microanatomy and antioxidant system.

The human mind receives, perceives, and processes visual and auditory input daily from the everyday
world of art and culture as an esthetic neural experience involving several regions of the cerebrum.
It is important to comprehend how this process of neuroesthetics works and how it affects each
individual’s emotions and behavior. This article will incorporate various clinical scanning techniques
and methods to examine the anatomical cerebral structures where the effects of external neuroesthetic
stimuli can be correlated with its resultant neural cognitive response. The effects of neuroesthetic
stimuli on the clinical improvement in patients experiencing depression, cognitive decline, and
other forms of behavioral manifestations will be reviewed. The results of these studies (including
international examples, along with various comparative analyses) demonstrate the beneficial effects
of art on the pleasure centers of the brain and its consequent positive effects on patients’ behavior and
emotions, thus exemplifying the short‑ and long‑term importance of incorporation of neuroesthetics
in not only the clinical setting but also in our global society.

Recent years have seen a surge in psychiatric diseases, which has resulted in considerable disease
distress and considerably decreased living conditions. Many considerable synthetic medications have
been used to treat these illnesses throughout the years, but they have been found to have limited
effects and substantial recurrence risks in many individuals. Mental illnesses such as depression
and anxiety are persistently on the rise around the world, posing serious challenges to the affected
person’s and their family members’ personal lives. There is mounting evidence that suggests the gut–
brain axis (GBA) contributes to the genesis and development of psychiatric diseases. This review
focuses on contemporary dietary therapies such as Mediterranean diets and dietary supplements
and emphasizes nutrition’s critical role in psychiatric care through the GBA. Several research have
indicated that dietary quality affects mental health because it controls metabolic processes, has
anti‑inflammatory and antiapoptotic characteristics, and promotes neurogenesis and synaptogenesis.
This study demonstrates many dietary components, their relationships to depression, and how they
work. The use of dietary recommendations to support mental health appears to be a novel, affordable,
useful, nonpharmacological intervention for people with mental problems.

Background: Tramadol has a high potential for misuse resulting in cognitive impairment.
Zingiber officinale, however, possesses neuroprotective qualities. Objective: Microscopically
assessed hippocampal CA1 and CA3 following Z. officinale and tramadol treatment.
Materials and Methods: Two milliliters/kilogram of distilled water was given to Group 1,
Groups 2–5 were administered 50 mg/kg of tramadol while Group 3 was also administered 12.5 mg/
kg of naltrexone, and Groups 4 and 5 were also administered 500, and 1000 mg/kg ethanol extract of
Z. officinale (EEZO), respectively, orally for 21 days. The rats were euthanized and their brains were
collected, fixed in 10% formal saline, and processed routinely using crystal fast violet (CFV) stain for
the demonstration of Nissl substance, glial fibrillary acidic protein (GFAP) for the demonstration of
astrocytes, and Hematoxylin and Eosin for general histoarchitecture and estimation of cell number and
volume using physical dissector and Cavalieri estimator, respectively. Results: CFV stain revealed
alterations in regions of CA1 and CA3 of the hippocampus presenting as indistinct staining intensity
and peripheral Nissl substance accumulation in the tramadol‑treated group. GFAP revealed numerous
reactive astrocyte processes. The area of reactive astrocytes remarkably increased (P < 0.05) and
the intensity of the Nissl substance remarkably reduced in the tramadol-exposed group. When
compared to the control, the tramadol-exposed group’s hippocampal volume considerably (P < 0.05)
decreased (coefficient of error [CE] =0.050). The tramadol treatment group (CE = 0.090) relative to
the control group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal
cells in the CA3 region. The tramadol treatment group (CE = 0.090) compared to the control
group (CE = 0.060) showed a striking decrease (P < 0.05) in the number of pyramidal cells in the
CA3 region. Tramadol toxicity was attenuated in the groups treated with EEZO in a dose-dependent
manner. Conclusion: Z. officinale possesses a potential neuroprotective effect against tramadol‑induced
neurotoxicity.

Tumor necrosis factor (TNF) plays a role in host cell defense. TNF‑alpha (TNF‑α), secreted from
macrophage has an important role in proinflammatory response mechanism. TNF‑α levels increase in
autoimmune, systemic inflammatory diseases, especially rheumatological diseases. Therefore, TNF‑α
inhibitors are alternant in the treatment of many inflammatory diseases. TNF‑α inhibitors are not
the first choice of clinicians due to their important adverse effects, despite the fact that successful
results in diseases treatments. Treatment with TNF‑α inhibitors causes different adverse effects
including many bacterial, viral and fungal infectious diseases, lung diseases, demyelinating diseases,
and malignancies. One of the most important adverse effect is tuberculosis (TB) by Mycobacterium
tuberculosis bacillus. TB occurs through reactivation in Latent TB infection. Thus, TB screening
tests appliedbefore TNF‑α inhibitors treatment have an importance. In this review, TNF‑α inhibitors
and their important adverse effect TB flaming were discussed, and also genetic background features
of these molecules have been explained.

In this review, the biological structure of garlic, its active ingredients, especially allicin and its way
of antimicrobial effects on cells evaluated and also the toxic possibility of allicin on diverse cells was
investigated. Various academic papers have been found in reliable literature. It is stated that garlic
includes lots of phytoconstituents with activities against cells. The toxic action of allicin on different
cell lines such as bacteria kinds such as Gram-positive (Staphylococcus aureus, Bacillus subtilis,
Streptococcus pneumoniae) and Gram-negative bacteria (Klebsiella pneumoniae, Helicobacter pylori,
Escherichia coli, Pseudomonas aeruginosa) for all that fungi like Candida albicans and parasites,
virus, glioma and human neuroblastoma cell lines and also oral tongue squamous cell carcinoma,
cancer cell lines which are characterized as malignant (leukemia, colon, gastric, and breast cell
lines) cancer. It has been revealed that, on those cells, allicin has also been demonstrated toxicity
mechanisms on cells like canceling deed of nitric oxide synthase, the peroxidation of lipids, nuclear
factor, kappa B, arranging cell period, modulating the activity of redox precision proteins and
influence cellular signaling.