Introduction:  Benzodiazepines are a class of sedative-hypnotic drugs often used by people suffering from anxiety, sleep disorders, stress reactions, panic disorders, obsessive-compulsive disorders, and mania due to their anticonvulsant, anxiolytic, and muscle relaxant properties [1,2]. Between the year 1996 to 2013, the percentage of US adults filling benzodiazepine prescriptions rose from 8.1 million to 13.5 million (67% increase), and the cumulative quantity of benzodiazepines served over the years surged by 140% [3]. However, this rise in treatment using benzodiazepines heavily contributed to an increase in the number of cases of benzodiazepine overdose-related deaths, from 0.58 to 3.07 per 100,000 adults. This value soon reached a plateau in early 2010 but continued to increase among the elderly and the Hispanic and African American communities [3]. It is worth noting that nearly 75% of these deaths were not caused by benzodiazepines alone but by the added effects of alcohol, opioids, or amphetamines [3].In mention to its relation with age, the use and misuse of benzodiazepines vary, with individuals between the ages of 50 to 64 years having the highest prescription-based use, whereas young adults of ages 18 to 25 years presented with the highest statistics for non-prescription based use, highlighting the misuse and abuse of benzodiazepines, according to a study conducted in the United States [4].Overdoses induced by benzodiazepines rarely present as an emergency and are often aggravated further by additional ingestion of other drugs [5]. In people with long-term benzodiazepine use, immediate retirement from the drug may induce a severe withdrawal syndrome, resulting in anxiety, confusion, sleep disorders, and in extreme cases, seizures [6]. The most widely used benzodiazepine, Alprazolam, has much greater side effects from withdrawal, including mania, psychosis, delirium, and hyperadrenergic states [7]. Furthermore, tapering of benzodiazepines has been linked to Takotsubo cardiomyopathy [8].This article reports a case regarding a Pakistani patient with no previous history of drug abuse that voluntarily overdosed on benzodiazepines (Alprazolam) alone and was later diagnosed with hypoxic-ischemic (anoxic) encephalopathy.Case Presentation:A 32-year-old Pakistani male was presented to the emergency department in an unconscious and gasping condition. His mother had found him in an unresponsive, comatose state. The patient had a history of epilepsy, anxiety, and depression. The remainder of his past medical history was unremarkable, and any admissions made during childhood had no recrudesce in adulthood.At the emergency department, the patient suffered multiple seizure episodes, and remained unconscious, maintaining a GCS of 3/15. Upon physical examination, unresponsive bilateral pinpoint pupils were noted; the neck of the patient was found to be supple, and the bilateral plantar reflexes were normal, suggesting active involuntary movement. His abdomen was soft and nontender, and his chest was found to be unremarkable.On the first day of admission, a complete blood count revealed a low hemoglobin count of 12.9 g/dl, leukocytosis (white blood cell count of 14.0 x 10^9/L), neutrophilia (neutrophil at 93%), hyperglycemia (glucose concentration at 93 mg/dl) and hyperproteinemia (proteins: 66.1 mg/dl), while displaying a minor decrease in the hematocrit levels. The test for plasma lactate levels was normal, resting at 15.5; however, lactate dehydrogenase levels produced a low result of 21 U/L (the normal range is 135 – 225 U/L). The above-mentioned laboratory investigations have been summarized in Table 1. Arterial blood gases revealed high anion gap metabolic acidosis. On the second day of admission, a urine test revealed a positive result for benzodiazepine overdose (>200 ng/ml) while testing negative for amphetamines, cannabinoids, barbiturates, and cocaine metabolites, as mentioned in Table 2.  Enzyme-linked immunosorbent assay for human immunodeficiency virus (HIV) antibodies and tests for the presence of Hepatitis B and C virus revealed negative results. The gram stain showed no organisms. On the fifth day, a test for C-reactive protein (CRP) revealed a CRP of 15.62 mg/l (normal range is less than 6), suggesting the presence of an inflammation reaction. His respiratory examination displayed acute hypercapnic respiratory failure (type II).A CT scan, which was also conducted on the first day, revealed no intraparenchymal hemorrhage, cerebral edema, or midline shift. Grey and white matter differentiation were intact, and the basal ganglia and thalami showed normal density. This was viewed through multiple axial images obtained from the base up to the vertex of the skull without intravascular contrast.Initial treatment for hypercapnic respiratory failure and seizures was initiated, as these were the presenting symptoms when our patient had arrived in the ER. He was intubated, aided by a pressure-synchronized intermittent mandatory ventilation (P-SIMV) mode ventilator, and transferred to the ICU for intensive care and monitoring. The patient was administered anti-inflammatory glucocorticoids, intravenous lactam antibiotics (meropenem, and tazobactam with piperacillin), levetiracetam for the treatment of seizures, and half normal saline with 2 amps of KCL at 75 ml/hr via a nasogastric tube as an immediate course of treatment.On the third day, the patient had self-extubated but maintained an oxygen saturation of 99% and was supplied with 5 L/min oxygen via facemask at a respiratory rate of 22/min. The patient’s GCS topped 15/15, and reintubation was considered unnecessary. The patient was drowsy, but was physically responsive and fully capable of conversing with the consultant. On this day the patient was diagnosed with benzodiazepine poisoning. The patient admitted to intentionally overdosing on Alprazolam, a type of benzodiazepine, with suicidal intentions, despite not having any history of using the drug or any other illicit substances previously. He was later diagnosed with major depressive disorder by the neurologist that overlooked the case.Further in regards to the patient’s condition, anion gaps returned to normal, and no further seizures occurred. The patient remained fatigued, but mobilization out of bed was prescribed. The patient had a physiotherapy session in which chest physiotherapy was conducted. The patient was kept in an ICU setting for another day before being transferred to a normal monitoring setup.In regards to the radiological tests taken following the initial CT scan, an echocardiography, electroencephalography (EEG) and a general abdomen ultrasound were taken on the third day. Echocardiography revealed atypical septal motion and an ejection fraction of 55%; however, all other findings were normal, with an absence of thrombi or pericardial effusions. EEG reported fast beta activity of 15-18 Hz in the background rhythm and muscle stiffness due to ventilation; however, photic stimulation was normal, and no focal or generalized epileptic discharges were noted. Since idiopathic epilepsy appears normal on an interictal EEG, the technician had advised that a diagnosis be made after clinical correlation. The abdominal ultrasound showed a slightly altered texture with raised echogenicity of the liver; however, the rest of the abdomen was unremarkable. On the fifth and sixth days of admission, a brain MRV/DWI and MRA were conducted to accurately view the condition of the brain. MRA revealed a comparatively attenuated right vertebral artery with normal hyperintensity within the right and left vertebral, basilar, and bilateral posterior cerebral arteries. No evidence of stenosis or abnormal dilation of the hyperintense arteries was seen. The MRV presented evidence of bilateral symmetrical abnormal signal intensity areas seen in the basal ganglia, predominantly in the globus pallidus, which appears hyperintense on T2/FLAIR images while showing restriction on the DWI images. The superior sagittal, inferior sagittal, transverse, and straight sinuses appeared unremarkable, and no venous segment filling was detected to show signs of thrombosis. Another MRV, which was taken 24 hours after the first one, presented the Dural sinuses as normal. The MRI, MRA, and MRV imaging, with DWI protocol, demonstrates ischemic hypoxic insult involving bilateral globus pallidus, which was later understood to be linked to the benzodiazepine intoxication.Upon gaining consciousness, the patient admitted to intentionally overdosing on Alprazolam with suicidal intentions, despite not having any history of using the drug or any other illicit substances previously. He was later diagnosed with major depressive disorder by the neurologist that overlooked the case.On the final day, the patient possessed the following vitals: blood pressure of 130/80, a pulse of 76/min, respiratory rate of 21/min, and oxygen saturation of 99% in the absence of oxygen support. The abdomen, respiratory and cardiovascular examinations were completely normal. The patient had fully gained consciousness, was well-oriented in time, place, and person, and held a GCS of 15/15, with an attenuated right vertebral artery under CNS findings. He was discharged after staying at the hospital for 6 days and was instructed to return for a follow-up after 1 week.During the follow-up, the patient presented with no cognitive deterioration and was completely responsive and healthy. The patient presented with no personality changes and sustained a GCS of 15/15.