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Early consciousness recovery after cardiac arrest (CA) is one of the most explicit and self-evident prognostic factors for clinical outcomes. We aimed to evaluate the prognostic value of electroencephalography (EEG) phenotypes according to the American Clinical Neurophysiology Society’s Critical Care EEG classification for predicting early recovery after CA.
Consecutive patients admitted to the ICU after CA were enrolled. We analyzed Glasgow Coma Scale (GCS) score within 10 days after CA and evaluated mortality within 28 days according to EEG pattern subtype.
Among the total of 71 patients, 9 had periodic discharges (PDs) EEG pattern, 4 had rhythmic delta activity (RDA), 8 had spike-and-wave (SW), 22 had low voltage, 5 had burst suppression, and 23 had other EEG patterns. Initial GCS scores, GCS scores 3 days after CA (or 3 days after targeted temperature management [TTM]), and 10 days after CA (or 10 days after TTM) were significantly different among EEG subtypes (p < 0.001, respectively) (Table 2). GCS scores were significantly higher in RDA and the other EEG group compared to the PDs, SW, low voltage, and burst suppression groups (p < 0.001). Significant group × time interactions were observed for the follow-up period between EEG phenotypes (p < 0.001) demonstrating the most increase in the other EEG pattern group.
Consciousness states were significantly worse in the PDs, SW, burst suppression, and low-voltage groups compared to the RDA and the other EEG pattern within 10 days after CA. The degree of consciousness recovery differed significantly by EEG pattern subtype within 10 days.
Patients with an equivalent clinical background may show unexpected interindividual differences in their outcome. The cognitive reserve (CR) model has been proposed to account for such discrepancies, but its role after acquired severe injuries is still being debated. We hypothesize that inappropriate investigative methods might have been used when dealing with severe patients, which have very likely reduced the possibility of observing meaningful influences in recovery from severe traumas.
To overcome this issue, the potential neuroprotective role of CR was investigated, considering a wider spectrum of clinical symptoms ranging from low-level brain stem functions necessary for life to more complex motor and cognitive skills. In the present study, data from 50 severe patients, 20 suffering from post-anoxic encephalopathy (PAE) and 30 with traumatic brain injury (TBI), were collected and retrospectively analyzed.
We found that CR, diagnosis, time of hospitalization, and their interaction had an effect on the clinical indexes. When the predictive power of CR was investigated by means of two machine learning classifier algorithms, CR, together with age, emerged as the strongest factor in discriminating between patients who reached or did not reach successful recovery.
Overall, the present study highlights a possible role of CR in shaping the recovery of severe patients suffering from either PAE or TBI. The practical implications underlying the need to routinely considered CR in the clinical practice are discussed.
Nivolumab has become an effective treatment option for cancer in various sites; however, this drug may cause immune-related adverse effects due to its mechanism of action. Furthermore, little has been reported on thiamine deficiency (TD) in patients receiving nivolumab treatment.
From a series of cancer patients, we reported a patient with recurrent renal cell carcinoma who developed TD after the start of nivolumab treatment.
A 74-year-old man with recurrent renal cell carcinoma was referred to the psycho-oncology department as he had lost about 4 kg and displayed a loss of energy after four cycles of nivolumab treatment. Psychiatric interviews revealed a decrease in energy. Neurological examination did not reveal any impairment in consciousness, ataxia, or ocular symptoms. He did not develop appetite loss. The malabsorption or overconsumption of some nutrients is thought to occur due to the rapid loss of weight; thus, a reduction in vitamin B1, which has a short storage period in the body and is often deficient in cancer patients, was suspected. The diagnosis of TD was supported by the patient's abnormally low serum thiamine level.
Significance of results
In patients treated with nivolumab, it is necessary to pay careful attention to TD when proceeding with the treatment. It is hoped that future research may reveal the link between nivolumab administration and TD.
A 59-year-old man presented with confusion, decreased level of consciousness, and generalized tonic–clonic seizures. He was intubated and promptly stabilized on antiepileptic medications. He was not in status epilepticus. He improved after seizure control, though he remained confused. He was neither acutely intoxicated nor were there any substance withdrawal concerns prior to his presentation. Furthermore, no metabolic, electrolyte, or nutritional perturbations were identified. He did, however, have a history of alcoholic hepatitis and was awaiting a liver transplant, but his blood work did not reveal evidence of fulminant hepatic failure at presentation (international normalized ratio – 1.17, platelet count 161,000/µL, ammonia 18 µmol/L, blood urea nitrogen 4.5 mmol/L, and his liver enzymes were only remarkable for an elevated alkaline phosphatase of 143 U/L).
Thiamine deficiency (TD) is recognized in various kinds of disease with associated loss of appetite including cancer. However, it has not been recognized to date in bereaved partners after spousal loss from cancer.
From a series of bereaved partners who lost a spouse to cancer, we report on those who developed TD after bereavement.
Case 1 was a 57-year-old woman who sought consultation at our “bereavement clinic.” Her husband had been diagnosed with pancreatic cancer one year earlier and had died one month previously. At the first visit, she was observed to suffer depression, anxiety, and decreased appetite. Neurological, blood, and biochemical examinations did not reveal any noteworthy findings. She was diagnosed with uncomplicated bereavement. Detailed examination revealed that her appetite had been markedly decreased for approximately five weeks. The diagnosis of TD was supported by her abnormally low serum thiamine level. Case 2 was a bereaved 73-year-old male who had lost his wife to hypopharyngeal cancer one month previously after a five-year illness. He had shown a lack of energy for the month preceding his wife's death, but because there was no improvement after her death, his family recommended he seek consultation at our “bereavement clinic.” He was suffering from major depressive disorder. Detailed examination revealed that his appetite had been decreased for more than two weeks. Again, the diagnosis of TD was supported by his abnormally low serum thiamine level.
Significance of results
These reports demonstrate that there is a possibility that bereaved could develop TD after the loss of a loved one. TD should be considered whenever there is a loss of appetite lasting for more than 2 weeks, and medical staff should pay careful attention to the physical condition of the bereaved to prevent complications because of TD.
Thiamine deficiency (TD) is recognized in various kinds of disease with associated loss of appetite including cancer; however, TD has not been recognized in the family caregivers of cancer patients to date.
From a series of cancer patient caregivers, we reported an aged family caregiver who developed TD while caring for the cancer patient.
The caregiver was a 90-year-old male. He had been accompanying his wife, who was diagnosed with colon cancer 4 years previously, on hospital visits as the primary caregiver, but because of psychological issues, he was recommended to visit the psycho-oncology department's “caregiver's clinic” for a consultation. Detailed examination revealed that his appetite had been only about 50% of usual from about one year before, and he had lost 12 kg in weight in one year. The diagnosis of TD was supported by his abnormally low serum thiamine level.
Significance of the results
This report demonstrates that there is a possibility that care providers could develop TD from the burdens associated with caregiving. TD should be considered whenever there is a loss of appetite lasting for more than 2 weeks, and medical staff should pay careful attention to the physical condition of care providers to prevent complications resulting from TD.
Although thiamine deficiency (TD) and Wernicke encephalopathy (WE) are not rare in cancer patients, the cases reported to date developed TD and/or WE after treatment had started.
From a series of cancer patients, we report a patient diagnosed with TD without the typical clinical symptoms of WE at the preoperative psychiatric examination.
A 43-year-old woman with ovarian cancer was referred by her oncologist to the psycho-oncology outpatient clinic for preoperative psychiatric evaluation. Her tumor had been growing rapidly before the referral. Although she did not develop delirium, cerebellar signs, or eye symptoms, we suspected she might have developed TD because of her 2-month loss of appetite as the storage capacity of thiamine in the body is approximately 18 days. The diagnosis of TD was supported by abnormally low serum thiamine levels.
Significance of results
Cancer therapists need to be aware that thiamine deficiency may occur even before the start of cancer treatment. In cases with a loss of appetite of more than 2 weeks’ duration, in particular, thiamine deficiency should be considered if the tumor is rapidly increasing, regardless of the presence or absence of delirium.
Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency. It is recognized in various stages of the cancer trajectory but has not previously been recognized during nivolumab treatment.
From a series of WE patients with cancer, we report a lung cancer patient who developed WE during treatment with nivolumab.
A 78-year-old woman with lung cancer was referred to our psycho-oncology clinic because of depressed mood. Psychiatric examination revealed disorientation to time, date, and place, which had not been recognized 1 month previously. Her symptoms fulfilled the diagnostic criteria for delirium. No laboratory findings or drugs explaining her delirium were identified. WE was suspected as she experienced a loss of appetite lasting 4 weeks. This diagnosis was supported by abnormal serum thiamine and the disappearance of delirium after intravenous thiamine administration.
Significance of results
We found WE in an advanced lung cancer patient receiving treatment with nivolumab. Further study revealed the association between nivolumab and thiamine deficiency. Oncologists should consider thiamine deficiency when a patient experiences a loss of appetite of more than 2 weeks regardless of the presence or absence of delirium.
Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency, and is sometimes overlooked because of the diversity of clinical symptoms.
From a series of WE patients with cancer, we report a lung cancer patient who developed WE, the main symptom of which was agitation.
A 50-year-old woman with lung cancer was referred to our psycho-oncology clinic because of agitation lasting for three days. No laboratory findings or drugs explaining her agitation were identified. Although the patient did not develop delirium, ophthalmoplegia, or ataxia, WE was suspected because she experienced a loss of appetite loss lasting 5 weeks. This diagnosis was supported by abnormal serum thiamine and disappearance of agitation one hour after intravenous thiamine administration.
Significance of results
This report emphasizes the clinical diversity of WE and indicates the limits of the ability to diagnose WE from typical clinical symptoms. The presence of a loss of appetite for more than two weeks may be the key to the accurate diagnosis of WE.
Thiamine is an essential coenzyme for oxidative metabolisms; however, it is not synthesized in the human body, and the average thiamine storage capacity is approximately 18 days. Therefore, thiamine deficiency (TD) can occur in any condition of unbalanced nutrition. If TD is left untreated, it causes the neuropsychiatric disorder Wernicke encephalopathy (WE). Although WE is a medical emergency, it is sometimes overlooked because most patients with WE do not exhibit all of the typical symptoms, including delirium, ataxia, and ophthalmoplegia. If all of the typical clinical symptoms of WE are absent, diagnosis of TD or WE becomes more difficult.
From a series of cancer patients, we reported three patients who developed TD without the typical clinical symptoms of WE.
A 69-year-old woman with pancreatic body cancer receiving chemotherapy with paclitaxel and gemcitabine for six months. Her performance status (PS) was 1. A detailed interview revealed that she had appetite loss for six months. Another 69-year-old woman with ovarian cancer received nedaplatin; her PS was 0. A detailed interview revealed that she had appetite loss for three months. A 67-year-old woman with colon cancer receiving ramucirumab in combination with second-line fluorouracil with folinic acid and irinotecan. Her PS was 1. A detailed interview revealed that she had appetite loss for three weeks. None exhibited typical clinical signs of WE, but they developed appetite loss for six months, three months, and three weeks, respectively. The diagnosis of TD was supported by abnormally low serum thiamine levels.
Significance of the results
This report emphasizes the possibility of TD in cancer patients even when patients do not develop typical clinical signs of WE. The presence of appetite loss for more than two weeks may aid in diagnosing TD. Patients receiving chemotherapy may be at greater risk for developing TD.
Background: Secondary neurotransmitter deficiencies have been reported in several reviews. Our primary aim was to assess the relationship among epilepsy, antiseizure medications, and specific neurotransmitter abnormalities. We also evaluated movement disorders and brain abnormalities via magnetic resonance imaging scans in patients with secondary neurotransmitter defects. Methods: This is a retrospective case series of 376 patients who underwent neurotransmitter analysis at BC Children’s Hospital between 2009 and 2013, for a variety of neurological presentations. The biochemical genetics laboratory database was interrogated for results of cerebrospinal fluid neurotransmitter analyses. Clinical data for patients with abnormal results were collected from the hospital charts. Statistical analysis included one-way analysis of variance, chi-square, and a two-way contingency table. Results: Abnormal neurotransmitter values were identified in 67 (17.8%) patients, two (0.53%) of which were attributable to a congenital neurotransmitter disorder and 11 (16.9%) secondary to other genetic diagnoses. Of 64 patients with secondary abnormal neurotransmitter values, 38 (59%) presented with epilepsy and 20 (31%) with movement disorders. A combination of epilepsy and movement disorder was less frequent. Discussion: Acknowledging the limitations of this retrospective chart review, we conclude that, in our cohort, in addition to patients with movement disorders, a considerable number of patients with epilepsy and epileptic encephalopathy also showed secondary neurotransmitter mono-amine abnormalities. There is no clear relation, however, between clinical phenotype and type of neurotransmitter affected. In addition, no association was identified between the type of antiseizure medications and affected neurotransmitter type. We outline the need for prospective studies to further enrich our understanding of the relation between epilepsy and neurotransmitters with a focus on improving treatments and patient outcomes.
Headache is an uncommon symptom in Guillain–Barré syndrome (GBS). We review four clinical settings related to GBS in which headache may be present. We focus on pathophysiological explanations, alerting the clinician to further potential investigations and treatment. Most reports of headache in GBS occur in the context of the posterior reversible encephalopathy syndrome, an increasingly recognized dysautonomia-related GBS complication. Less frequent is headache in the setting of increased intracranial pressure and papilledema (secondary intracranial hypertension), Miller Fisher syndrome, and cerebral venous sinus thrombosis. Rarely, headache can occur secondary to aseptic meningitis from IVIg use.
Occasional cases of classical bovine spongiform encephalopathy (BSE) still continue to occur within the European Union (EU) for animals born after reinforced feed bans (BARBs), which should in theory have eliminated all risk of infection. The study aimed to determine (i) whether a common rate of decline of BSE infection was evident across EU member states, i.e. to determine whether control measures have been equally effective in all member states, (ii) whether there was any evidence of spontaneous occurrence of BSE in the data and (iii) the expected date for the last BSE case in UK. It was found that there was no significant difference in the rate of decline of BSE prevalence between member states, with a common rate of decline of 33·9% per annum (95% CI 30·9–37%) in successive annual birth cohorts. Trend analysis indicated an ultimate decline to 0 prevalence, suggesting that spontaneous occurrence does not explain the majority of cases. Projecting forward the trends from the back-calculation model indicated that there was approximately a 50% probability of further cases in the UK, and should the current rate of decline continue, there remains the possibility of further occasional cases up until 2026.
Wernicke encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine deficiency. Several reports of WE in cancer patients are known. WE is sometimes overlooked because most patients do not exhibit its typical symptoms (e.g., delirium, ataxia, ocular palsy). If delirium is not present, a diagnosis of WE is difficult because delirium is the hallmark symptom of WE.
Taken from a series on WE in cancer, we report two patients who developed WE without delirium during periodic psycho-oncology outpatient visits.
Case 1. A 61-year-old woman with non-Hodgkin lymphoma who was periodically attending a psycho-oncology outpatient clinic developed an unsteady gait. WE was suspected because she also developed appetite loss for two weeks, and we could find no other laboratory findings to explain her unsteady gait. Our diagnosis was supported by abnormal serum thiamine and disappearance of the gait disturbance after intravenous thiamine administration. Case 2. A 50-year-old woman with breast carcinoma with bone metastasis developed an unsteady gait. WE was suspected because she also developed loss of appetite for two weeks, and no other laboratory findings could explain her unsteady gait. The diagnosis was supported by abnormal serum thiamine and disappearance of the gait disturbance after administration of intravenous thiamine.
Significance of Results:
Our report emphasizes the importance of being aware of WE, even when patients do not present with delirium. The presence of loss of appetite for more than two weeks may be the key to a diagnosis of WE.