An important challenge in brain research is to make out the relation between the features of olfactory stimuli and the electroencephalogram (EEG) signal. Yet, no one has discovered any relation between the structures of olfactory stimuli and the EEG signal. This study investigates the relation between the structures of EEG signal and the olfactory stimulus (odorant). We show that the complexity of the EEG signal is coupled with the molecular complexity of the odorant, where more structurally complex odorant causes less fractal EEG signal. Also, odorant having higher entropy causes the EEG signal to have lower approximate entropy. The method discussed here can be applied and investigated in case of patients with brain diseases as the rehabilitation purpose.
A patient with severe hyponatreamia secondary to chronic renal failure was treated with peritoneal dialysis (PD). On the third day of admission, she developed progressive obtundation. Neurological examination showed bilateral brisk reflexes with intact brain stem reflexes. Magnetic resonance imaging demonstrated patchy demyelination of the pontine area indicating central pontine myelinolysis (CPM). Despite supportive measures, the patient died on the fifteenth day of admission. The rate of correction of hyponatraemia with peritoneal dialysis can be rapid and detrimental to hyponatraemic chronic renal failure patients and careful monitoring of serum sodium level is advocated.
A prospective study was carried out to determine the incidence, clinical presentation, early outcome, and risk factors associated with periventricular haemorrhage (PVH) in 88 (84 per cent) of the 105 consecutive very low birth weight (VLBW) (< 1500 g) Malaysian neonates born in the Maternity Hospital, Kuala Lumpur. Based on the cranial ultrasound findings, PVH was detected in 86 of the 88 neonates (98 per cent, 95 per cent confidence intervals: 95 to 101). Seventeen (20 per cent) of them had grade I, 52 (61 per cent) had grade II, 7 (8 per cent) had grade III and 10 (12 per cent) had grade IV PVH. PVH was detected in all the affected neonates by the fifth day of life. Sixty-four neonates (74 per cent) were symptomatic when PVH was first detected. Shock (P < 0.01), pallor (P = 0.028), low haematocrit of less than 40 per cent (P < 0.01), convulsion (P < 0.001), and bulging of anterior fontanelle (P = 0.019) were significantly more common in the neonates with severe PVH (grades III or IV). Death occurred in 43/86 (50 per cent, 95 per cent confidence interval: 39-61 per cent) of the neonates with PVH before their first discharge from the hospital. Ventriculomegaly developed in 29/43 (67 per cent, 95 per cent confidence intervals: 54.4-81.4) of the survivors with PVH. Our study suggests that PVH is a common problem in the Malaysian VLBW neonates. To reduce the incidence and severity of this condition, prevention of preterm delivery and improvement in the basic facilities for neonatal care would help.
Long-COVID is a postviral illness that can affect survivors of COVID-19, regardless of initial disease severity or age. Symptoms of long-COVID include fatigue, dyspnea, gastrointestinal and cardiac problems, cognitive impairments, myalgia, and others. While the possible causes of long-COVID include long-term tissue damage, viral persistence, and chronic inflammation, the review proposes, perhaps for the first time, that persistent brainstem dysfunction may also be involved. This hypothesis can be split into two parts. The first is the brainstem tropism and damage in COVID-19. As the brainstem has a relatively high expression of ACE2 receptor compared with other brain regions, SARS-CoV-2 may exhibit tropism therein. Evidence also exists that neuropilin-1, a co-receptor of SARS-CoV-2, may be expressed in the brainstem. Indeed, autopsy studies have found SARS-CoV-2 RNA and proteins in the brainstem. The brainstem is also highly prone to damage from pathological immune or vascular activation, which has also been observed in autopsy of COVID-19 cases. The second part concerns functions of the brainstem that overlap with symptoms of long-COVID. The brainstem contains numerous distinct nuclei and subparts that regulate the respiratory, cardiovascular, gastrointestinal, and neurological processes, which can be linked to long-COVID. As neurons do not readily regenerate, brainstem dysfunction may be long-lasting and, thus, is long-COVID. Indeed, brainstem dysfunction has been implicated in other similar disorders, such as chronic pain and migraine and myalgic encephalomyelitis or chronic fatigue syndrome.
We describe four families with affected siblings showing unique clinical features: early-onset (before 1 year of age) progressive diffuse brain atrophy with regression, postnatal microcephaly, postnatal growth retardation, muscle weakness/atrophy, and respiratory failure. By whole-exome sequencing, we identified biallelic TBCD mutations in eight affected individuals from the four families. TBCD encodes TBCD (tubulin folding co-factor D), which is one of five tubulin-specific chaperones playing a pivotal role in microtubule assembly in all cells. A total of seven mutations were found: five missense mutations, one nonsense, and one splice site mutation resulting in a frameshift. In vitro cell experiments revealed the impaired binding between most mutant TBCD proteins and ARL2, TBCE, and β-tubulin. The in vivo experiments using olfactory projection neurons in Drosophila melanogaster indicated that the TBCD mutations caused loss of function. The wide range of clinical severity seen in this neurodegenerative encephalopathy may result from the residual function of mutant TBCD proteins. Furthermore, the autopsied brain from one deceased individual showed characteristic neurodegenerative findings: cactus and somatic sprout formations in the residual Purkinje cells in the cerebellum, which are also seen in some diseases associated with mitochondrial impairment. Defects of microtubule formation caused by TBCD mutations may underlie the pathomechanism of this neurodegenerative encephalopathy.