Yusari, I Gusti Agung Ayu Andra
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PSEUDOBULBAR AFFECT AND COGNITIVE DECLINE POST SEVERE TRAUMATIC BRAIN INJURY: A CASE REPORT Yusari, I Gusti Agung Ayu Andra; Laksmidewi, Anak Agung Ayu Putri
MNJ (Malang Neurology Journal) Vol. 10 No. 2 (2024): July
Publisher : PERDOSSI (Perhimpunan Dokter Spesialis Saraf Indonesia Cabang Malang) - Indonesian Neurological Association Branch of Malang cooperated with Neurology Residency Program, Faculty of Medicine Brawijaya University, Malang, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.mnj.2024.010.02.15

Abstract

Introduction: Pseudobulbar affect is described as episodes of laughing or crying that occur suddenly and uncontrollably without appropriate stimulation. Pseudobulbar affect is often preceded by various neurological disorders, one of which is a history of severe head injury. Case Report: Female, 21 years old, experienced sudden frequent laughing for no apparent reason and could not be controlled. This has been happening after she suffered a severe head injury, which was a subarachnoid hemorrhage, about two years ago. She was diagnosed with pseudobulbar affect according to Cummings criteria and confirmed by Center for Neurologic Study – Lability Scale (CNS-LS) questionnaire with a score of 19. The patient also complained of forgetting things, therefore a cognitive function was examined with Indonesian Version of the Montreal Cognitive Assessment (MoCA-Ina) with a score of 14 which indicated moderate cognitive impairment. Discussion: Pseudobulbar affect post traumatic brain injury is suspected to be caused by decreased inhibition of sensory cortex transmission to the motor cortex and limbic system leading to disturbances in the cerebellum and decreased threshold for emotional expression. Pseudobulbar affect may coexist with impaired cognitive function due to the intersection of the anatomical structure of cognitive function with pathways that regulate emotion. Conclusion: Pseudobulbar affect with cognitive impairment creates a burden and interferes the patient’s quality of life. It is necessary for health workers to be able to identify the clinical manifestations of pseudobulbar affect as a complication after traumatic brain injury, therefore optimal management for the patients can be achieved.
Todd’s Paresis as a Postictal Phenomenon in Post-Traumatic Epilepsy: A Case Report Yusari, I Gusti Agung Ayu Andra; Susilawathi, Ni Made; Mahadewi, Ni Putu Ayu Putri
AKSONA Vol. 5 No. 2 (2025): JULY 2025
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/aksona.v5i2.54758

Abstract

Highlight: Todd’s paresis presented as transient hemiparesis in a case of untreated post-traumatic epilepsy. Proposed pathomechanisms of Todd’s paresis include neuronal exhaustion, active inhibition, and postictal hypoperfusion. Todd’s paresis was commonly misdiagnosed as acute ischemic stroke due to the similar clinical presentation   ABSTRACT Introduction: Todd’s paresis is defined as a paralysis state after an epileptic seizure that lasts for several hours to days and recovers completely afterwards. It usually manifests as a transient hemiparesis after a focal or generalized seizure. Todd’s paresis cases and its mechanisms were still widely discussed. Case: A 48-year-old man with history of post-traumatic epilepsy presented with right-sided hemiparesis and facial weakness after a general motor tonic-clonic seizure. The location of the hemiparesis was contralateral to the post-trauma lesion in left frontal lobe which was suspected to be the focus of the seizure. The postictal weakness resolved completely after 30 hours without any specific intervention. It was revealed that the patient had been having several seizures beforehand after the epidural and subdural hematoma due to head trauma. The patient was diagnosed as Todd’s paresis following a post ictal condition in patient with post-traumatic epilepsy. Conclusion: Todd’s paresis should be considered as a diagnosis in patients with seizure and stroke-like syndrome such as hemiparesis due to its similar manifestations, especially if it resolves within hours. Several mechanisms were suggested to be the pathophysiology of Todd’s paresis including neuronal exhaustion, active inhibition, and postictal hypoperfusion.