A rare case of rickettsial fever with isolated third cranial nerve palsy causing hemophagocytic lymphohistiocytosis

Rickettsial infections are being increasingly diagnosed in the Indian subcontinent with the advent of affordable and sensitive diagnostic techniques. Rickettsial infections are sometimes complicated by the development of secondary hemophagocytic lymphohistiocytosis (HLH) which is life-threatening unless identified early and treated. Here, we describe a case of rickettsial fever in a 41-year-old male who presented with fever, skin rash, and neurological obtundation, complicated by both third cranial nerve palsy and HLH. The patient showed a good recovery in sensorium with intravenous doxycycline and dexamethasone, although the oculomotor nerve palsy persisted for about two months after discharge. This case highlights the need to initiate treatment for rickettsial fever and HLH on clinical grounds before waiting for confirmation by laboratory tests.

Transient third cranial nerve palsy after pipeline shield treatment of a ruptured anterior cerebral artery dissecting aneurysm: Case report

Background: Intracranial dissecting aneurysms (IDAs) are rare vascular lesions usually arising from the posterior circulation. The anterior cerebral artery (ACA) is an unusual location for this pathology. Even rarer is the occurrence of a transient de novo third cranial nerve (CN) palsy after flow-diverting device (FDD) treatment of an ACA dissecting aneurysm. Case Description: A middle-aged man with a prior history of hypertension was admitted to our emergency department with severe headache and loss of consciousness after sexual intercourse. Imaging revealed a subarachnoid hemorrhage with stenosis of the left A1 segment of the ACA. Cerebral digital subtraction angiography confirmed a dissecting aneurysm of the left A1 segment. The aneurysm was treated with an FDD (Pipeline Shield). Transient isolated incomplete third CN palsy was documented 12 h after treatment. No evidence of ischemic or hemorrhagic strokes was found. The condition improved after a few days of empiric steroid treatment. Conclusion: An FDD is a suitable alternative for the treatment of a ruptured IDA of the anterior circulation. Some infrequent complications associated with the device, such as de novo cranial neuropathies, are yet to be studied.

Chronic subdural hematoma

Chronic subdural hematoma (CSH) is a common neurosurgical pathology that is recognized as a consequence of minor head injuries that are usually diagnosed in senile patients, although it can occur in young patients without a history of trauma. The objective of this work is the presentation of a patient with a bilateral CSH, with unusual characteristics. Clinical case: a 46-year-old female patient with no history of head trauma or other concomitant pathology is presented, who consulted for a 15-day-old headache. Physical examination confirmed mydriasis, Hutchinson’s pupil, bilateral papilledema and exophoria of the right eye, third cranial nerve palsy, and trunk ataxia. She was cataloged with Glasgow 13. Early anti-cerebral edema treatment was performed and the manifestations largely disappeared. A computed tomography scan diagnosed a bilateral fronto temporal subdural hematoma with displacement of the midline structures to the left. She underwent emergency surgery and was discharged completely recovered three days later. Conclusion: HSC can present with different clinical forms, simulating expansive tumor processes, cerebrovascular attacks, dementias or neurological entities of another nature. The case management by clinicians and neurosurgeons was quick and effective, which explains that the patient had an early and complete recovery. In these cases, medical action is decisive in the success of the treatment.

Chronic subdural hematoma

Chronic subdural hematoma (CSH) is a common neurosurgical pathology that is recognized as a consequence of minor head injuries that are usually diagnosed in senile patients, although it can occur in young patients without a history of trauma. The objective of this work is the presentation of a patient with a bilateral CSH, with unusual characteristics. Clinical case: a 46-year-old female patient with no history of head trauma or other concomitant pathology is presented, who consulted for a 15-day-old headache. Physical examination confirmed mydriasis, Hutchinson’s pupil, bilateral papilledema and exophoria of the right eye, third cranial nerve palsy, and trunk ataxia. She was cataloged with Glasgow 13. Early anti-cerebral edema treatment was performed and the manifestations largely disappeared. A computed tomography scan diagnosed a bilateral fronto temporal subdural hematoma with displacement of the midline structures to the left. She underwent emergency surgery and was discharged completely recovered three days later. Conclusion: HSC can present with different clinical forms, simulating expansive tumor processes, cerebrovascular attacks, dementias or neurological entities of another nature. The case management by clinicians and neurosurgeons was quick and effective, which explains that the patient had an early and complete recovery. In these cases, medical action is decisive in the success of the treatment.

Clinical Significance of Isolated Third Cranial Nerve Palsy in Traumatic Brain Injury: A Detailed Description of Four Different Mechanisms of Injury through the Analysis of Our Case Series and Review of the Literature

Third cranial nerve palsy (3cnP) following traumatic brain injury (TBI) is a worrying neurological sign and is often associated with an expanding mass lesion, such as extradural or acute subdural haematomas. Isolated 3cnP can be found in the absence of posttraumatic space-occupying mass lesion, yet it is often considered as a devastating prognostic factor in the context of diffuse axonal injury (DAI). Through the analysis of five exemplificative cases and a thorough review of the literature, we identified four possible mechanisms leading to 3cnP: (1) a partial rootlet avulsion at the site of exit from the midbrain, representing a direct shearing injury to the nerve; (2) a direct traction injury due to the nerve stretching against the posterior petroclinoid ligament at the base of the oculomotor triangle secondary to the downward displacement of the brainstem at the time of impact; (3) a direct vascular compression as a result of internal carotid artery (ICA) dissection or pseudoaneurysm; (4) an indirect injury caused by impaired blood supply to the third nerve in addition to the detrimental biochemical effects of the underlying brain injury itself. Understanding the exact mechanism underlying the onset of 3cnP is key to provide an informed clinical decision-making to the patients and ensure their best chances of recovery. Our experience corroborates data from the literature showing that, even in Grade III DAI, prompt recognition of isolated 3cnP can guide adequate treatment. Nonetheless, even when an overall good neurological outcome is achieved, recovery of isolated 3cnP is dismal, and only rarely the visual deficit completely resolves.