Psychoactive Plant Database - Neuroactive Phytochemical Collection

1. Cureus. 2024 Nov 6;16(11):e73132. doi: 10.7759/cureus.73132. eCollection 2024 
Nov.

Effective Pain Management of Postherpetic Neuralgia Using a Combination of 
Analgesics and Conservative Measures.

Tsubaki T(1), Kodaka E(2), Kitano Y(2), Kodama M(3), Fukumoto S(4), Takano C(5), 
Iino S(2), Hirono Y(1).

Author information:
(1)Surgery, Cancer Care Promotion Center, University of Fukui Hospital, Fukui, 
JPN.
(2)Dermatology, Faculty of Medical Sciences, University of Fukui, Fukui, JPN.
(3)Palliative Care, Cancer Care Promotion Center, University of Fukui Hospital, 
Fukui, JPN.
(4)Neuropsychiatry, Faculty of Medical Sciences, University of Fukui, Fukui, 
JPN.
(5)Nursing, University of Fukui Hospital, Fukui, JPN.

Postherpetic neuralgia (PHN) is characterized by persistent pain following the 
resolution of a herpes zoster rash. PHN is often resistant to treatment and can 
significantly reduce the patient's quality of life. Effective symptom relief is 
crucial and various treatments, including pharmacotherapy, have been attempted. 
Given that symptoms can persist for a prolonged period, they can substantially 
affect the physical and mental well-being of the patients. A 73-year-old man 
developed herpes zoster while undergoing treatment for a head angiosarcoma. 
Despite the resolution of the rash, the pain persisted, leading to the diagnosis 
of PHN. Treatment was initiated with a range of medications, including 
mecobalamin, pregabalin, and a combination of tramadol and acetaminophen, along 
with general pain relievers standardized as WHO Step 1 medications, which 
include acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs). 
However, achieving adequate pain control is challenging and results in frequent 
hospitalizations. Due to the patient's depression and the concurrent use of a 
selective serotonin reuptake inhibitor, duloxetine hydrochloride could not be 
prescribed. Instead, opioid therapy with continuous fentanyl citrate infusion 
was initiated. Eventually, the treatment was switched to oxycodone 
hydrochloride, which successfully stabilized the patient's symptoms. The use of 
conservative measures such as hot compresses also contributes to symptom relief. 
Alleviating pain symptoms using a combination of pharmacotherapeutic and 
non-pharmacological treatments is extremely important.

Copyright © 2024, Tsubaki et al.

DOI: 10.7759/cureus.73132
PMCID: PMC11539919
PMID: 39507605

Conflict of interest statement: Human subjects: Consent was obtained or waived 
by all participants in this study. Conflicts of interest: In compliance with the 
ICMJE uniform disclosure form, all authors declare the following: 
Payment/services info: All authors have declared that no financial support was 
received from any organization for the submitted work. Financial relationships: 
All authors have declared that they have no financial relationships at present 
or within the previous three years with any organizations that might have an 
interest in the submitted work. Other relationships: All authors have declared 
that there are no other relationships or activities that could appear to have 
influenced the submitted work.


2. Sci Rep. 2024 Nov 6;14(1):26949. doi: 10.1038/s41598-024-78528-7.

40 Hz light preserves synaptic plasticity and mitochondrial function in 
Alzheimer's disease model.

Barzegar Behrooz A(1)(2)(3), Aghanoori MR(1)(4)(5), Nazari M(1)(6), Latifi-Navid 
H(2)(4)(7), Vosoughian F(1), Anjomani M(1), Lotfi J(8)(9), Ahmadiani A(1), 
Eliassi A(1)(2), Nabavizadeh F(2)(10), Soleimani E(1), Ghavami S(#)(11)(12)(13), 
Khodagholi F(#)(1), Fahanik-Babaei J(#)(14).

Author information:
(1)Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, 
Tehran, Iran.
(2)Electrophysiology Research Center, Neuroscience Institute, Tehran University 
of Medical Sciences, Tehran, Iran.
(3)Department of Human Anatomy and Cell Science, College of Medicine, University 
of Manitoba, Winnipeg, MB, Canada.
(4)Department of Molecular Medicine, National Institute of Genetic Engineering 
and Biotechnology (NIGEB), Tehran, Iran.
(5)Department of Medical Genetics, Cumming School of Medicine, University of 
Calgary & Alberta Children's Hospital Research Institute, Calgary, AB, T2N 4N1, 
Canada.
(6)Department of Physiology, Faculty of Medicine, Arak University of Medical 
Sciences, Arak, Iran.
(7)School of Biological Sciences, Institute for Research in Fundamental Sciences 
(IPM), Tehran, Iran.
(8)Department of Clinical Biochemistry, Faculty of Medical Sciences, Tarbiat 
Modares University, Tehran, Iran.
(9)Growth and Development Research Center, Tehran University of Medical 
Sciences, Tehran, Iran.
(10)Department of Physiology, School of Medicine, Tehran University of Medical 
Sciences, Tehran, Iran.
(11)Faculty of Medicine in Zabrze, University of Technology in Katowice, Zabrze, 
41-800, Poland.
(12)Research Institute of Oncology and Hematology, Cancer Care 
Manitoba-University of Manitoba, Winnipeg, MB, Canada.
(13)Children Hospital Research Institute of Manitoba, University of Manitoba, 
Winnipeg, MB, Canada.
(14)Electrophysiology Research Center, Neuroscience Institute, Tehran University 
of Medical Sciences, Tehran, Iran. Fahanikbabaei1358@gmail.com.
(#)Contributed equally

Alzheimer's disease (AD) is the most prevalent type of dementia. Its causes are 
not fully understood, but it is now known that factors like mitochondrial 
dysfunction, oxidative stress, and compromised ion channels contribute to its 
onset and progression. Flickering light therapy has shown promise in AD 
treatment, though its mechanisms remain unclear. In this study, we used a rat 
model of streptozotocin (STZ)-induced AD to evaluate the effects of 40 Hz 
flickering light therapy. Rats received intracerebroventricular (ICV) STZ 
injections, and 7 days after, they were exposed to 40 Hz flickering light for 
15 min daily over seven days. Cognitive and memory functions were assessed using 
Morris water maze, novel object recognition, and passive avoidance tests. 
STZ-induced AD rats exhibited cognitive decline, elevated reactive oxygen 
species, amyloid beta accumulation, decreased serotonin and dopamine levels, and 
impaired mitochondrial function. However, light therapy prevented these effects, 
preserving cognitive function and synaptic plasticity. Additionally, flickering 
light restored mitochondrial metabolites and normalized ATP-insensitive 
mitochondrial calcium-sensitive potassium (mitoBKCa) channel activity, which was 
otherwise downregulated in AD rats. Our findings suggest that 40 Hz flickering 
light therapy could be a promising treatment for neurodegenerative disorders 
like AD by preserving synaptic and mitochondrial function.

© 2024. The Author(s).

DOI: 10.1038/s41598-024-78528-7
PMID: 39506052 [Indexed for MEDLINE]


3. Psychiatr Clin North Am. 2024 Dec;47(4):723-739. doi:
10.1016/j.psc.2024.04.014.  Epub 2024 May 28.

Childhood Anxiety Disorders.

Stiede JT(1), Mangen KH(2), Storch EA(2).

Author information:
(1)Baylor College of Medicine, One Baylor Plaza, 1977 Butler boulevard, Suite 
4-400, Houston, TX 77030, USA. Electronic address: jordan.stiede@bcm.edu.
(2)Baylor College of Medicine, One Baylor Plaza, 1977 Butler boulevard, Suite 
4-400, Houston, TX 77030, USA.

Anxiety disorders are common in children and adolescents, with many youths 
experiencing functional impairment in multiple domains because of these 
conditions. Biologic and cognitive-behavioral models provide a basis for the 
development and maintenance of these disorders. Cognitive behavioral therapy 
(CBT) with exposures and selective serotonin reuptake inhibitors or serotonin 
and norepinephrine reuptake inhibitors are empirically supported treatments for 
childhood anxiety disorders. Exposures are a key component of CBT treatment and 
a case vignette demonstrates how to tailor exposures to the unique fears of the 
child.

Copyright © 2024 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.psc.2024.04.014
PMID: 39505450 [Indexed for MEDLINE]

Conflict of interest statement: Disclosure J.T. Stiede and K.H. Mangen have no 
disclosures to report. E.A. Storch reports receiving research funding to his 
institution from the REAM Foundation, United States, International OCD 
Foundation, United States, and NIH, United States. He was a consultant for 
Brainsway and Biohaven Pharmaceuticals in the past 12 months. He owns stock less 
than $5000 in NView. He receives book royalties from Elsevier, Wiley, Oxford, 
American Psychological Association, Guildford, Springer, and Jessica Kingsley.


4. Psychiatr Clin North Am. 2024 Dec;47(4):689-709. doi:
10.1016/j.psc.2024.04.012.  Epub 2024 Jun 10.

Pharmacotherapy for Anxiety Disorders.

O'Leary KB(1), Khan JS(2).

Author information:
(1)Menninger Department of Psychiatry & Behavioral Sciences, Baylor College of 
Medicine, 1 Baylor Plaza - BCM350, Houston, TX 77030, USA. Electronic address: 
Kerry.O'Leary@bcm.edu.
(2)Menninger Department of Psychiatry & Behavioral Sciences, Baylor College of 
Medicine, 1977 Butler Boulevard, E4.203. Houston, TX 77030, USA.

Anxiety disorders are the most common psychiatric illness and include disorders 
such as generalized anxiety disorder (GAD), panic disorder (PD), and social 
anxiety disorder (SAD). Psychotherapy and pharmacotherapy are both effective 
treatments for anxiety disorders, with efficacy between 60% and 85%. Selective 
serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors 
are first-line pharmacologic treatment for GAD, PD, and SAD. Recommendations for 
treating pediatric and geriatric populations vary slightly, but first-line 
treatments remain the same. Recent advancements in the treatment of anxiety 
disorders are limited although research has discovered novel pathways, which may 
lead to additional treatment options in the future.

Copyright © 2024 Elsevier Inc. All rights reserved.

DOI: 10.1016/j.psc.2024.04.012
PMID: 39505448 [Indexed for MEDLINE]

Conflict of interest statement: Disclosure The authors have nothing to disclose.


5. Mol Cell Biochem. 2024 Nov 6. doi: 10.1007/s11010-024-05153-3. Online ahead of
 print.

Novel hypothesis and therapeutic interventions for irritable bowel syndrome: 
interplay between metal dyshomeostasis, gastrointestinal dysfunction, and 
neuropsychiatric symptoms.

Nakagawa Y(1), Yamada S(2).

Author information:
(1)Center for Pharma-Food Research (CPFR), Division of Pharmaceutical Sciences, 
Graduate School of Integrative Pharmaceutical and Nutritional Sciences, 
University of Shizuoka, 52-1 Yada, Suruga-Ku, Shizuoka, 422-8526, Japan. 
gp1958@u-shizuoka-ken.ac.jp.
(2)Center for Pharma-Food Research (CPFR), Division of Pharmaceutical Sciences, 
Graduate School of Integrative Pharmaceutical and Nutritional Sciences, 
University of Shizuoka, 52-1 Yada, Suruga-Ku, Shizuoka, 422-8526, Japan.

Irritable bowel syndrome is a gastrointestinal disorder due to multiple 
pathologies. While patients with this condition experience anxiety and depressed 
mood more frequently than healthy individuals, it is unclear how 
gastrointestinal dysfunction interacts with such neuropsychiatric symptoms. Data 
suggest that irritable bowel syndrome patients predominantly display a lower 
zinc intake, which presumably impairs enterochromaffin cells producing 
5-hydroxytryptamine, gut bacteria fermenting short-chain fatty acids, and 
barrier system in the intestine, with the accompanying constipation, diarrhea, 
low-grade mucosal inflammation, and visceral pain. Dyshomeostasis of copper and 
zinc concentrations as well as elevated pro-inflammatory cytokine levels in the 
blood can disrupt blood-cerebrospinal fluid barrier function, leading to locus 
coeruleus neuroinflammation and hyperactivation with resultant amygdalar 
overactivation and dorsolateral prefrontal cortex hypoactivation as found in 
neuropsychiatric disorders. The dysregulation between the dorsolateral 
prefrontal cortex and amygdala is likely responsible for visceral pain-related 
anxiety, depressed mood caused by anticipatory anxiety, and visceral pain 
catastrophizing due to catastrophic thinking or cognitive distortion. 
Collectively, these events can result in a spiral of gastrointestinal symptoms 
and neuropsychiatric signs, prompting the progression of irritable bowel 
syndrome. Given that the negative feedback mechanism in regulation of the 
hypothalamic-pituitary-adrenal axis is preserved in a subset of neuropsychiatric 
cases, dorsolateral prefrontal cortex abnormality accompanied by 
neuropsychiatric symptoms may be a more significant contributing factor in 
brain-gut axis malfunction than activation of the hypothalamic 
corticotropin-releasing hormone system. The proposed mechanistic model could 
predict novel therapeutic interventions for comorbid irritable bowel syndrome 
and neuropsychiatric disorders.

© 2024. The Author(s), under exclusive licence to Springer Science+Business 
Media, LLC, part of Springer Nature.

DOI: 10.1007/s11010-024-05153-3
PMID: 39503802