The Protean Neuropsychiatric and Vestibuloauditory Manifestations of Neurosarcoidosis

2017 ◽  
Vol 22 (4-5) ◽  
pp. 205-217 ◽  
Author(s):  
Jacqueline J. Greene ◽  
Ilka C. Naumann ◽  
Janet M. Poulik ◽  
Kevin T. Nella ◽  
Lindsay Weberling ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Implantation ◽  
Psychiatric Symptoms ◽  
Altered Mental Status ◽  
Rapid Onset ◽  
Normal Serum ◽  
High Dose ◽  
Leptomeningeal Enhancement ◽  
History Of

Background: A rare subset of sarcoidosis, neurosarcoidosis, is reported to occur in 5-7% of sarcoid patients and can manifest in a variety of ways. The most common are facial paralysis and optic neuritis, less commonly causing cochleovestibulopathy, blindness, anosmia, and other cranial nerve (CN) palsies. The sensory deficit may be severe and psychiatric symptoms may result from the effects of the disease or steroid treatment. Although MRI-compatible cochlear implants are now available, concerns about the feasibility of recoverable hearing with cochlear implantation in these patients as well as the practical difficulty of disease monitoring due to implant artifact must be considered. Results: We present 3 recent cases from different institutions. The first is a 39-year-old man with a history of progressively worsening hearing loss, followed by visual loss, delusions, agitation, ataxia, and musical auditory hallucinations, diffuse leptomeningeal enhancement on MRI with a normal serum angiotensin-converting enzyme (ACE) level but elevated cerebrospinal fluid (CSF) ACE levels, suggesting neurosarcoidosis, was treated with corticosteroids, and underwent successful cochlear implantation. The second is a 36-year-old woman with rapid-onset horizontal diplopia, left mixed severe sensorineural hearing loss (SNHL) and tinnitus, diffuse leptomeningeal enhancement on MRI, and progressive palsy of the left CNs IV, VI, VII, IX, X and XI, with altered mental status requiring admission following high-dose intravenous corticosteroids. The third is a 15-year-old boy who presented with sudden, bilateral, profound SNHL, recurrent headaches, and left facial weakness refractory to antivirals, ultimately diagnosed with neurosarcoidosis following an aborted cochlear implantation where diffuse inflammation was found, and histopathology revealed Schaumann bodies; he was treated with methotrexate and later underwent successful cochlear implantation. Conclusions: Neurosarcoidosis is an elusive diagnosis and can cause hearing loss and psychiatric symptoms. Cochlear implantation for patients with severe hearing loss should be considered once the diagnosis is confirmed, as it is possible to achieve a successful level of hearing. Psychiatric symptoms can manifest with the onset of neurosarcoidosis, result from CN deficits, or develop as a side effect from long-term, high-dose corticosteroids, and should be monitored carefully in patients with neurosarcoidosis.

LONG-TERM EFFECTS OF OTITIS MEDIA A TEN-YEAR COHORT STUDY OF ALASKAN ESKIMO CHILDREN

PEDIATRICS ◽  
1973 ◽  
Vol 52 (4) ◽  
pp. 577-585 ◽  
Author(s):  
Gary J. Kaplan ◽  
J. Kenneth Fleshman ◽  
Thomas R. Bender ◽  
Carol Baum ◽  
Paul S. Clark
Keyword(s):  
Hearing Loss ◽  
Otitis Media ◽  
Verbal Ability ◽  
Significant Loss ◽  
Long Term Effects ◽  
Normal Range ◽  
History Of ◽  
Conductive Component ◽  
Verbal Development

Histories of ear disease, otoscopic examinations, and audiologic, intelligence, and achievement tests were obtained from a cohort of 489 Alaskan Eskimo children who have been followed through the first ten years of life. Seventy-six per cent had experienced one or more episodes of otitis media since birth. Of these, 78% had their first attack during their first two years of life. Perforations and scars were present in 41%. A hearing loss of 26 decibels or greater was present in 16%, and an additional 25% were in the normal range but had a measurable air-bone gap. Children with a history of otitis media prior to 2 years of age and a hearing loss of 26 decibels or greater had a statistically significant loss of verbal ability and were behind in total reading, total math, and language. In addition, children who had an early onset of otitis media but now had normal hearing with a conductive component were also adversely affected in verbal areas. The number of otitis media episodes was related to tympanic membrane abnormalities, hearing loss, and low verbal and achievement scores. These findings indicate that otitis media has been a significant cause of morbidity in Alaskan Eskimo children, and its onset during the critical years of language development as well as the number of episodes play an important role in impairing verbal development.

scholarly journals Laporan Kasus: Manifestasi Oral Penderita Hipertensi berupa Ginggival Enlargement

2020 ◽  
Vol 17 (2) ◽  
pp. 54
Author(s):  
Anindita L. ◽  
Aris Aji K. ◽  
Arcadia Sulistijo J.
Keyword(s):  
Case Reports ◽  
Gingival Tissue ◽  
High Dose ◽  
Gingival Inflammation ◽  
Gingival Enlargement ◽  
History Of ◽  
Root Planning ◽  
Pro Inflammatory Cytokines

Hypertension presents an increase in blood pressure following the oral manifestations, such as gingival enlargement. A 42-year-old woman came to the General Sudirman University Dental and Oral Hospital complaining of enlarged front gums seven years ago. The patient had a history of hypertension and regularly consumed drugs, amlodipine 5 mg. Extraoral examination revealed no lymphadenopathy and no swelling of the head and neck area. Intraoral examination revealed a gingival enlargement involving the papilla to the gingival margin present on the entire upper and lower labial gingival surface. The patient's diagnosis was gingival enlargement caused by gingival enlargement due to the use of amlodipine. Gingival enlargement has been noted with long-term or high-dose amlodipine use. The mechanism of amlodipine in causing gingival enlargement is through the role of fibroblasts with abnormal susceptibility to the drug, resulting in increased levels of protein synthesis, especially collagen. The role of pro-inflammatory cytokines occurs through an increase in interleukin-1β (IL-1β) and IL-6 in the inflamed gingival tissue due to the gingival fibrogenic response to drugs. Therapies were DHE and scaling and root planning as phase I in periodontal treatment. Plaque elimination is vital to reduce gingival inflammation that may occur. Substitution of the drug amlodipine may be needed if there is no improvement. Based on case reports, hypertension patients who took amlodipine could have gingival enlargement. The therapy given was plaque elimination in the form of DHE and Scaling and regular check-ups with the dentist.

Graves’ Hyperthyroidism-Induced Psychosis Treated With Aripiprazole—A Case Report

2012 ◽  
Vol 26 (1) ◽  
pp. 59-61 ◽  
Author(s):  
Livia R. Macedo ◽  
Jehan Marino ◽  
Brady Bradshaw ◽  
Joseph Henry
Keyword(s):  
Atrial Fibrillation ◽  
Psychiatric Symptoms ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Long Term Effects ◽  
Free T4 ◽  
History Of ◽  
Antithyroid Peroxidase Antibody ◽  
First Time

Graves’ disease is an autoimmune syndrome with symptoms such as tachycardia, atrial fibrillation, and psychiatric symptoms. Limited evidence exists for the treatment of Graves’ hyperthyroidism-induced psychosis with atypical antipsychotics. A 47-year-old female with a psychiatric history of bipolar disorder presented for the first time to the psychiatric hospital. She was agitated and grossly psychotic with delusions. Electrocardiogram showed atrial fibrillation and tachycardia. Drug screen urinalysis was negative. Endocrine workup resulted in a diagnosis of Graves’ disease (thyroid-stimulating hormone [TSH]: 0.005 μIU/mL, triiodothyronine [T3]: 537 ng/dL, thyroxine [T4]: 24 mcg/dL, free T4: 4.5 ng/dL, positive antithyroid peroxidase antibody, and antinuclear antibody). Aripiprazole 10 mg daily was initiated and titrated to 15 mg daily on day 4. On day 16, her suspicious behavior, judgment, and insight improved. Other medications given included aspirin 325 mg daily, metoprolol 25 mg twice daily, titrated to 12.5 mg twice daily, and methimazole 30 mg daily, titrated to 20 mg twice daily, and discontinued on day 29. The patient received radioiodine I-131 treatment 1 week later. We report the first known case on the use of aripriprazole to treat Graves’ hyperthyroidism-induced psychosis. Further studies examining the long-term effects and appropriate dose and duration of aripiprazole in this patient population are needed.

Long-term health status of high-risk neuroblastoma survivors treated with high-dose chemotherapy and hematopoietic stem cell transplantation.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 10054-10054 ◽  
Author(s):  
Sandrine Haghiri ◽  
Chiraz Fayech ◽  
Christelle Dufour ◽  
Claudia Pasqualini ◽  
Stephanie Bolle ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Stem Cell ◽  
High Risk ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
High Dose Chemotherapy ◽  
High Dose ◽  
Second Cancers

10054 Background: Current treatment strategies including high-dose chemotherapy with stem cell transplantation rescue (HDC-SCT) have improved 5-year event-free survival for high-risk neuroblastoma (HRNB) patients, but with an increased risk of late treatment-related toxicities. Methods: Between 1980 and 2012, 439 children were treated for HRNB with HDC-SCT in Gustave Roussy (GR), among which 145 were alive and disease-free at 5-year post-SCT. Long-term health data have been collected for those 145 patients, prospectively within the long-term follow-up clinic in GR or retrospectively from pediatric consultations. Results: With a median follow-up post-SCT of 15 years (range 5-34), we observed 6 late relapses, 11 second cancers (including 3 papillary thyroid carcinomas; median delay = 20 years post-SCT [18-22]) and 9 deaths. Event-free and overall survival at 20-year post-SCT were 82% (95%CI = 70–90) and 89% (95%CI = 78–95), respectively. A second health event was observed in 135 patients (median = 3/patient), including 103 patients with at least 1 severe event (median = 1/patient). Cumulative incidence at 15-year post-SCT for second cancers is 4%, cardiac diseases 8%, thyroid 11%, renal 7%, hepatic focal nodular hyperplasia 14%, dental mal-development 70%, and severe hearing loss 20%. Height-for-age z-score was ≤-2 for 30 patients (21%) and ≤-3 for 12 patients (8%). After Busulfan-Melphalan conditioning regimen, 40/43 females and 33/35 males had a gonadal insufficiency. Conclusions: Long-term consequences of HRNB treatment including HDC are frequent and disabling, mainly due to hearing loss and gonadal insufficiency.

Possible Hepatotoxicity Associated With Daptomycin

2016 ◽  
Vol 29 (3) ◽  
pp. 253-256 ◽  
Author(s):  
Yoonsun Mo ◽  
Fletcher Nehring ◽  
Andrew H. Jung ◽  
Seth T. Housman
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Pain Syndrome ◽  
Liver Function Tests ◽  
Future Research ◽  
High Dose ◽  
History Of ◽  
The Relationship

Purpose To report a case of isolated daptomycin-induced acute liver injury without elevations in creatine kinase (CK) levels or kidney dysfunction. Summary A 49-year-old female with a history of pancreatitis, lupus, diabetes, congestive heart failure, hypertension, and chronic pain syndrome presented to the emergency department with alteration in mental status and acute liver failure. The patient had been treated with daptomycin for methicillin-resistant Staphylococcus aureus (MRSA) endocarditis for 3 weeks. After ruling out other possible etiologies, daptomycin was suspected as a cause of acute liver failure. Her liver failure resolved gradually following withdrawal of daptomycin. Conclusion Although hepatic abnormalities caused by daptomycin are rare, a handful of cases with daptomycin-induced liver injury have been reported in the literature. Of note, in most cases, patients on daptomycin therapy developed liver damage with elevations in CK levels. Our case report suggests possible severe liver injury associated with high-dose and long-term daptomycin treatment in the absence of rhabdomyolysis. Future research is warranted to further investigate the relationship between daptomycin use and liver injury, yet it is reasonable to monitor liver function tests at baseline and weekly thereafter along with CK levels, especially in patients requiring long-term daptomycin therapy.

scholarly journals The Long-Term Efficacy of Cochlear Implantation for Hearing Loss in Muckel-Wells Syndrome

2019 ◽  
Vol 15 (3) ◽  
pp. 454-458
Author(s):  
Bakushi Ogawa ◽  
◽  
Mitsuhiro Aoki ◽  
Hidenori Ohnishi ◽  
Toshimitsu Ohashi ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cochlear Implantation ◽  
Term Efficacy ◽  
Wells Syndrome

scholarly journals A Case of Psychosis Due to Acute Hypocalcemia From Hypoparathyroidism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A172-A173
Author(s):  
Joseph Theressa Nehu Parimi ◽  
John Chen Liu ◽  
Rajani Gundluru ◽  
Sowjanya Naha ◽  
Timur Gusov ◽  
...  
Keyword(s):  
Psychiatric Symptoms ◽  
Case Reports ◽  
Severe Depression ◽  
Altered Mental Status ◽  
Auditory Hallucinations ◽  
Psychotic Symptoms ◽  
Organic Psychosis ◽  
Neuropsychiatric Manifestations ◽  
History Of ◽  
Gait Abnormalities

Abstract A 61-year-old female with past medical history of depression, hypoparathyroidism (hypoPtH), and hypothyroidism had disappeared from her home and was found wandering a few hours away with persecutory delusions, visual and auditory hallucinations. Serum calcium (Ca) was 6.3 mg/dL (range 8.6–10.2), albumin 3.7 g/dL (range 3.5–5.2) and ionized Ca 0.89 mmol/L (range 1.12–1.30). She was admitted and treated with Ca and calcitriol. Work-up for altered mental status was negative except for hypocalcemia (hypoCa) and scattered bilateral basal ganglia calcifications (BGC) with cortical and subcortical frontal lobe calcifications on CT. Psychiatry diagnosed delirium due to hypoCa. Acute psychosis resolved once Ca levels improved. Diagnosis of idiopathic hypoPtH was in 1997. Her regimen included Ca citrate 1500mg daily and 10 mcg of Forteo twice daily. She had skipped her medications for at least 2 days prior to presentation. Her medical records revealed that she was seen for severe depression, progressive gait abnormalities, slowed movements, and imbalance, in 2015. CT scan and MRI brain showed BGC. Her son gave a history of multiple admissions for psychosis, violence, delusions with agitation, and wandering at times when the patient was hypoCa, which was diagnosed as schizophrenia. Neuropsychiatric disturbances are commonly associated with hypercalcemia. Review of literature found a few case reports of psychosis and hypoPtH 1,2 BGC is common in hypoPtH. Psychotic symptoms due to BGC include auditory hallucinations, delusions of influence, paranoid states, and complex perceptual distortions.3,5 HypoCa is associated with cognitive impairment. Neurological manifestations tend to improve with Ca correction, but psychiatric symptoms do not improve substantially.4,5 Further studies are needed in hypoPtH with BGC to appropriately diagnose organic psychosis. This is important in management of the vicious cycle of psychiatric illness leading to noncompliance resulting in psychosis. Prevention of BGC will play a key role. References: 1. Finan M, Axelband J. This is your brain on calcium: psychosis as the presentation of isolated hypoparathyroidism. Am J Emerg Med. 2014;32:945.e1-4. 2. Ang AW, Ko SM, Tan CH. Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism. Psychosom Med. 1995;57:299–302. 3. Burns K, Brodaty H. Fahr’s disease and psychosis. In: Sachdev PS, Keshavan MS, editors. Secondary schizophrenia. Cambridge: Cambridge University; 2010. p. 358–66. 4. Maiti A, Chatterjee S. Neuropsychiatric manifestations and their outcomes in chronic hypocalcaemia. J Indian Med Assoc. 2013;111:174–7. 5. Amara A, Novais C, Coelho M, Silva A, Curral R, Brandao I, Torres A. Organic psychosis due to hypoparathyroidism in an older adult: a case report. Braz. J. Psychiatry; 2016; 38(4)

scholarly journals A Case Report of Massive Acetaminophen Poisoning Treated with a Novel “Triple Therapy”: N-Acetylcysteine, 4-Methylpyrazole, and Hemodialysis

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Emily A. Kiernan ◽  
Julie A. Fritzges ◽  
Kathryn A. Henry ◽  
Kenneth D. Katz
Keyword(s):  
Emergency Department ◽  
Metabolic Acidosis ◽  
Triple Therapy ◽  
Complete Resolution ◽  
Altered Mental Status ◽  
Rapid Onset ◽  
Anion Gap ◽  
High Dose ◽  
Emergency Physicians ◽  
Transplant Center

Massive acetaminophen (N-acetyl-p-aminophenol; APAP) ingestion is characterized by a rapid onset of mitochondrial dysfunction, including metabolic acidosis, lactemia, and altered mental status without hepatotoxicity which may not respond to the standard doses of N-acetylcysteine (NAC). A 64-year-old woman without medical history presented comatose after an ingestion of 208 tablets of Tylenol PM™ (APAP 500 mg and diphenhydramine 25 mg). The initial APAP concentration measured 1,017 µg/mL (therapeutic range 10-30 µg/mL), and elevated anion gap metabolic acidosis, lactemia, and 5-oxoprolinemia were detected. High-dose intravenous (IV) NAC, 4-methylpyrazole (4-MP), and hemodialysis (HD) were initiated. She was transferred to a liver transplant center and continued both NAC and HD therapies until complete resolution of metabolic acidosis and coma without developing hepatitis. She was discharged without sequelae. This is the fourth highest APAP concentration recorded in a surviving patient. Moreover, this is the first report of a novel “triple therapy” using NAC, 4-MP, and HD in the setting of massive APAP ingestion that presents with coma, elevated anion gap metabolic acidosis, and lactemia. Emergency physicians should recognize these critically ill patients and consider high-dose NAC, 4-MP, and HD to be initiated in the emergency department (ED).

scholarly journals Emergence Delirium: Can Corticosteroids Contribute to It?

2020 ◽  
Vol 09 (04) ◽  
pp. 304-306
Author(s):  
Roger Esmel-Vilomara ◽  
Alejandro Cruz ◽  
Cristina Inoriza ◽  
Eva Andreu ◽  
Francisca Munar
Keyword(s):  
Risk Factor ◽  
Renal Biopsy ◽  
Psychiatric Symptoms ◽  
Therapeutic Option ◽  
Corticosteroid Treatment ◽  
High Dose ◽  
Emergence Delirium

AbstractWe report a case of emergence delirium after a propofol-based sedation for a renal biopsy in a teenager patient who had received high-dose and long-term corticosteroid treatment. Corticosteroid treatment is proposed as a possible risk factor for emergence delirium, although controlled studies are needed to assess this relationship. Although treatment for emergence delirium has not been well established, as described with steroid-induced psychiatric symptoms, antipsychotics could be a good therapeutic option.

Strychnine poisoning causing generalized tetanic spasm

2020 ◽  
pp. 10.1212/CPJ.0000000000000943
Author(s):  
Simon Winzer ◽  
Kristian Barlinn
Keyword(s):  
Brain Activity ◽  
Selective Inhibition ◽  
Muscle Contractions ◽  
Whole Body ◽  
High Dose ◽  
Repeated Testing ◽  
Limited Effect ◽  
First Line Therapy ◽  
History Of

A 55-year old male presented with spontaneous and stimulus-triggered tetanic-like activity of the whole body without losing consciousness or orientation (video, http://links.lww.com/CPJ/A196). There was no history of trauma, and clinical examination did not reveal any tetanus-prone wound. Electroencephalography showed no significant alteration in brain activity. Serial intravenous benzodiazepines showed limited effect. Frequency and duration of muscle contractions increased over time and led to severe hypoxemia requiring intubation and sedation with propofol for almost 24 hours followed by continuous infusion of midazolam. Daily sedation pauses revealed ongoing generalized muscle spasm triggered by tactile and auditory stimuli and severe vegetative dysregulation. Tetanus antibody level suggested long-term protection. On day 6, toxicology revealed toxic levels of strychnine in serum (180 ng/ml [toxicity > 75 ng/ml]) and urine (514 ng/ml [no toxicity level defined]). Repeated testing showed markedly declined strychnine levels in serum (2.8 ng/ml) and urine (1.1 ng/ml) on day 11. Sedation was ultimately stopped on day 10. Subsequently, the patient recovered completely and was discharged on day 25. Strychnine ingestion mode remained unclear. Generalized tetanic spasm with sustained alertness, presumably caused by selective inhibition of post-synaptic glycine receptors in the spinal cord, should trigger testing for strychnine poisoning.1,2 High-dose intravenous benzodiazepines are considered first-line therapy for controlling muscle spasms; however, in patients whose muscle contractions are refractory to benzodiazepines, sedation with propofol or barbiturates is deemed necessary.1

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