Case Reports in Neurological Medicine

Adverse drug reactions to commonly prescribed medications such as phenytoin, used for seizures, often go undetected due to various factors. This case report highlights a 52-year-old male diagnosed with late-onset epilepsy who was prescribed phenytoin. Despite the standard dosage, the patient experienced toxicity symptoms and a seizure, prompting admission for assessment. Laboratory tests and imaging were inconclusive, leading to a therapeutic drug monitoring (TDM) consultation, which revealed elevated phenytoin levels. Genetic testing for CYP2C9 polymorphisms was not feasible but noted as significant, especially in populations with higher prevalence. Phenytoin was tapered, leading to the patient’s gradual recovery upon discontinuation and transition to valproate. The Naranjo scale predicted potential adverse drug responses (ADRs). This case underscores the significance of TDM, genetic considerations in drug metabolism, and the need to be vigilant in treating epilepsy to prevent such adverse events.

We report a patient with a symptomatic intraluminal internal carotid artery thrombus clinically revealed by cerebral infarction. In the preoperative evaluation, it was revealed that essential thrombocythemia existed in the background. Therefore, medical treatment with antithrombotic agents in conjunction with hydroxycarbamide for essential thrombocythemia was initiated, but the thrombus was not dissolved by three weeks. At this time, the patient underwent carotid endarterectomy, which removed the thrombus completely with its adjacent plaque without any perioperative stroke. The possibility of essential thrombocythemia may also be kept in mind when an increased platelet count is observed in patients with internal carotid artery thrombus. It is a reasonable option to precede medical treatment, including anticoagulant therapy, by setting the time limit for surgical intervention in such a disease state.

Background. A penetrating head injury (PHI) refers to a situation where a projectile has breached the cranium but does not exit it. It constitutes about 0.4% of all head injuries. Several nonmissile materials inserting the skull have been reported. But to our knowledge, never before has any case of PHI caused by a hit of rake been reported. We report a first case of PHI caused by a rake in a child; then, we relate our experience with its management and discuss the relevant literature. Cases Description. A 5-year-old boy has been admitted with a rake embedded in his head. That occurred during a violent play with a neighbor. At presentation, the child was alert; there was no neurological deficit. The rake was embedded in the parietal regions on each side of the midline. The head Computed Tomography (CT) scan performed showed a biparietal hyperdensity from either side of the midline with a metal artifact. In the operating room, after a transversal incision joining the 2 tips of the object, we performed successively bone flaps; object extraction; debridement; duraplasty; and closing. The outcome was uneventful. Conclusion. This is the first case of PHI by a rake. The surgical management constitutes the main challenging point.

We report a very rare case of referred pain caused by greater occipital nerve (GON) entrapment, inducing spontaneous pain in the whole body as well as in the trigeminal nerve region of the face and head. It has already been reported that entrapment of the GON can induce referred pain in the ipsilateral limb as well as the ipsilateral hemiface. A 42-year-old female patient presented with chronic pain in her gums, jaw angle, submandibular region, retro-auricular suboccipital, and temporo-occipital vertex that had been ongoing for four years. As the patient’s head pain and facial pain became severe, severe spontaneous pain occurred in the arm, waist, and both lower extremities. This patient’s pain in the occipital and neck, spontaneous pain in the face, jaw, and whole body improved with decompression of the GON. Anatomical basis of pain referral to the facial trigeminal area caused by chronic GON entrapment is convergence of nociceptive inflow from high cervical C1–C3 structures and trigeminal orofacial area in the dorsal horn of the cervical spinal cord from the C2 segment up to the medullary dorsal horn (MDH). The major afferent contribution among the suboccipital and high cervical structure is mediated by spinal root C2 that is peripherally represented by the GON. Chronic noxious input from GON entrapment can cause sensitization and hypersensitivity in second order neurons in the trigeminocervical complex (TCC) and MDH in the caudal trigeminal nucleus and high cervical cord. Generalized extension of referred pain due to GON entrapment is thought to involve two possible pathophysiologies. One is the possibility that generalized pain is caused by sensitization of third-order nociceptive neurons in the thalamus. Another speculation is that spontaneous pain may occur throughout the body due to dysfunction of the descending brain stem pain-modulating pathway by sensitization and hyperexcitation of the MDH and trigeminal brainstem sensory nuclear complex (TBSNC).

While the systemic effects of digoxin have been studied, limited data exist on the effects of neuraxial administration. Prior case reports document how digoxin and lidocaine share indistinguishable vials and were inadvertently stocked together in spinal and epidural anesthesia kits, necessitating a need for further implementation of safety measures. Here, we report the poor progression and brain death of a postpartum woman after accidental administration of intrathecal digoxin during a routine elective cesarean section (C-section). It is imperative that quality improvement and safety measures are taken to avoid the recurrence of this medical error.

Alzheimer’s disease (AD) is classified as a tauopathy and is the most common neuropathological correlate of dementia/cognitive impairment. AD is neuropathologically characterized by the presence of beta-amyloid immunoreactive senile plaques and tau positive neurofibrillary tangles. Neuropsychiatric symptoms of AD however continue to be underscored, and therefore, neuropathological correlates of these neuropsychiatric symptoms are not readily studied. Presented here is a case of 60-year-old female who initially presented with anxiety and depression, and continued to be the predominant symptoms although mild cognitive impairment was noted as per the available clinical notes. Postmortem examination of the brain revealed severe Alzheimer’s type neuropathological changes, which included significant tau and beta-amyloid pathology in limbic regions, which were thought to represent correlates of the patient’s depression and anxiety. This case report illustrates the possible neuropathological correlates of neuropsychiatric symptoms in patients with AD. The author hopes that such a case will promote more in-depth studies into the pathophysiology of neuropsychiatric manifestations in AD.