The management of elderly bipolar patients can become very complex due to higher prevalence of medical comorbidities and sensitivity to treatment-related adverse effects. One of the antiepileptic drugs used for their treatment, carbamazepine, has had a number of cognitive and psychomotor effects linked to it: deterioration in measures of information processing speed, and attention and faster motor skills after discontinuation, among others. The literature concerning them is quite sparse.

We report the case of a 75-year-old woman with bipolar disorder and unspecified cognitive impairment who was brought to the emergency department by her family due to global functional decline dating 3 weeks back.

The patient had been diagnosed and in treatment with bipolar disorder for 40 years. About 2 months before the current episode, because of the presence of tremor and family reports of marked functional decline (from being independent for daily life activities to being bound to a wheelchair and with worsening cognitive symptoms), the psychiatrist opted for a gradual switch from valproate to carbamazepine. During our interview, her husband pointed to the complete dose of 100 mg of carbamazepine 3 weeks ago as the onset of her current symptoms. The patient demonstrated clear psychomotor inhibition, with an absence of spontaneous movement and sporadic, almost monosyllabic, responses to only the simplest questions. Although aware that she was in a hospital, she could not recall its name and was completely disoriented in regards to time. Barely capable of emoting with her facial muscles, she denied feeling depressed and only acknowledged a stomachache. After spending the night in observation, and the suspension of carbamazepine, the patient experienced an improvement of her cognitive functions: although still not fully oriented in space and time, she could now speak in sentences and answer most of our questions. Even though she still maintained not being depressed, when pressed about any weird sensations she admitted to the feeling of being dead inside. The decision was made to transfer her to the psychogeriatric hospitalization unit.

The initial assessment of the patient was complicated due to a variety of factors. Beyond the physical comorbidities, the psychomotor inhibition impeded a thorough examination of her emotional state. Only the suppression of her evening dose of carbamazepine allowed for the diagnosis of Cotard-like major depressive symptoms. Even though the cognitive impairment was apparent before, the state of the patient was markedly improved with just the removal of carbamazepine and was confirmed by her family to be a lot closer to her base state of more than a month ago.

The use of anticonvulsant therapy in elderly bipolar patients with cognitive impairment can have important side effects. Further evidence of the prevalence and specific nature and frequency of its side effects is needed.

No Funding

On June 14, 2018, the FDA approved generic buprenorphine/naloxone, as an alternative to the brand Suboxone (FDA,2018). A patient who developed acute withdrawal symptoms when switched from Suboxone to generic buprenorphine/naloxone at the same dosage, with resolution with replacement with brand name Suboxone, is presented. Induction of withdrawal with generic buprenorphine/naloxone has not heretofore been described.

Case Study: A 39-year-old right handed single male presented with a past medical history of intravenous heroin dependence. He was relapse free for 5 years and without change on Suboxone film 8mg/2mg twice daily, and was provided with prescriptions for the same, which was substituted to generic brand Dr. Reddy’s Lab SA buprenorphine HCl/naloxone HCl 8mg/2mg film. After two days on this, one hour after taking generic buprenorphine/naloxone film, symptoms of withdrawal began as manifest by hot flashes, diaphoresis, cold chills, leg cramping, and nausea without vomiting. These were the same symptoms he experienced during his past inpatient withdrawal from opioids. These symptoms recurred every day for an entire week until switching back to brand name Suboxone, whereupon his withdrawal symptoms resolved.

The mechanism whereby the generic buprenorphine/naloxone combination induced withdrawal symptoms is unclear. It appears that this generic version was either not effectively blocking the mu receptors or the naloxone was inducing a withdrawal state. Possibly the porous nature of the film was such that less of the buprenorphine was absorbed through the mucosa. As a result, less was transferred into the bloodstream, across the blood brain barrier, to the nucleus accumbens, and ultimately on kappa opioid/mu receptor (Centerwatch, 2002). Alternatively, a greater amount of naloxone may have been absorbed transmucosally, thus inducing withdrawal. The absorption may have been normal, but the exact milligram dosage may not be accurate with either too little buprenorphine or too much naloxone. On the other hand, this buprenorphine compound may have been pH sensitive, such that it became inactivated upon exposure to the mildly acidic salivary pH. He could have been malingering this response. Again this is unlikely since he was not given a higher dose of buprenorphine/naloxone, rather the same dose of Suboxone as previously prescribed. It is important that physicians be aware of the possibility for acute withdrawal and increased cravings, which can lead to relapse while using this agent. Further investigation of the efficacy of the generic variant and Suboxone as replacement therapy is warranted.

The COVID-19 pandemic substantially impacted care of patients with schizophrenia treated with long-acting injectable antipsychotics (LAIs). This study examined how clinics adapted operations to maintain a standard of care for these patients after pandemic onset.

Online surveys were completed in October-November 2020 by one principal investigator (PI) or PI-appointed designee at 35 clinics participating in OASIS (NCT03919994). Items concerned pandemic impacts on clinic operations, particularly telepsychiatry, and on the care of patients with schizophrenia treated with LAIs.

All 35 clinics reported using telepsychiatry; 20 (57%) implemented telepsychiatry after pandemic onset. Telepsychiatry visits increased from 12%-15% to 45%-69% across outpatient visit types after pandemic onset; frequency of no-show and/or canceled telepsychiatry visits decreased by approximately one-third. Nearly half of clinics increased the frequency of telepsychiatry visits for patients with schizophrenia treated with LAIs. Approximately one-third of participants each reported switching patients treated with LAIs to longer injection interval LAIs or to oral antipsychotics. The most common system/clinic- and patient-related barrier for telepsychiatry visits was lower reimbursement rate and access to technology/reliable internet, respectively. Almost all participants (94%) were satisfied with telepsychiatry for maintaining care of patients with schizophrenia treated with LAIs; most predicted a hybrid of telepsychiatry and office visits post-pandemic.

Changes made by clinics after pandemic onset were viewed by almost all participants as satisfactory for maintaining a standard of care for patients with schizophrenia treated with LAIs. Most participants predicted continuing telepsychiatry to support patient care post-pandemic; equitable access to telepsychiatry will be important in this regard.

Alkermes, Inc.

To understand that tinnitus may be an aura for sleep paralysis.

Sleep paralysis is a transient-paralysis which occurs during awakening or falling asleep (Wilson, 1928). Those affected experience symptoms including visual, auditory, and haptic hallucinations, voluntary motor paralysis with intact ocular and respiratory motor movements, and diffuse or localized paresthesias. Sleep paralysis associated with tinnitus as an aura, has not heretofore been described.

A 34 year-old, right-handed female presented with a 13 year history of sleep paralysis. One month prior, she began to notice tinnitus prior to the onset of sleep paralysis. The tinnitus was bilateral, high-pitched, with a volume intensity of 5/10, lasting seven seconds prior to sleep initiation. She denied hearing loss, vertigo, dizziness, cataplexy, deja vu and jamais vu. After termination of tinnitus, she experienced paresthesia, “like at a dentist’s office” radiating from her posterior neck, to her tongue and down to her toes. She described seeing a white-shadowy male figure moving around her room, lasting seven seconds. Accompanied by a masculine “ahh” sound, lasting for three seconds. The sleep paralysis occurred after these events, lasting up to eight hours, or until her husband wakes her.

Abnormalities in Physical Examination: General Examination: right arm hemangioma 4 by 5cm. Reflexes: absent bilateral brachioradialis, 1+ bilateral quadriceps femoris and bilateral Achilles tendon. Neuropsychiatric Examination: Calibrated Finger Rub Auditory Screening Test: faint 70 AU (normal).

Tinnitus has been described as an aura for migraines (Schankin, 2014), temporal lobe epilepsy (TLE) (Florindo, 2006), and narcolepsy-cataplexy (Marco, 1978). These epochs may represent amigranous migraines, which initially present with tinnitus that occurs both during the day and night, forcing the patient to be partially awoken at night with induction of the sleep paralysis sequence. It would be worthwhile to query those with narcolepsy or sleep paralysis if tinnitus precedes the event.

Behaviors typical of body-focused repetitive behavior disorders such as trichotillomania (TTM) and skin-picking disorder (SPD) are often associated with pleasure or relief, and with little or no physical pain, suggesting aberrant pain perception. Conclusive evidence about pain perception and correlates in these conditions is, however, lacking.

A multisite international study examined pain perception and its physiological correlates in adults with TTM (n = 31), SPD (n = 24), and healthy controls (HCs; n = 26). The cold pressor test was administered, and measurements of pain perception and cardiovascular parameters were taken every 15 seconds. Pain perception, latency to pain tolerance, cardiovascular parameters and associations with illness severity, and comorbid depression, as well as interaction effects (group × time interval), were investigated across groups.

There were no group differences in pain ratings over time (P = .8) or latency to pain tolerance (P = .8). Illness severity was not associated with pain ratings (all P > .05). In terms of diastolic blood pressure (DBP), the main effect of group was statistically significant (P = .01), with post hoc analyses indicating higher mean DBP in TTM (95% confidence intervals [CI], 84.0-93.5) compared to SPD (95% CI, 73.5-84.2; P = .01), and HCs (95% CI, 75.6-86.0; P = .03). Pain perception did not differ between those with and those without depression (TTM: P = .2, SPD: P = .4).

The study findings were mostly negative suggesting that general pain perception aberration is not involved in TTM and SPD. Other underlying drivers of hair-pulling and skin-picking behavior (eg, abnormal reward processing) should be investigated.