INTRODUCTION
The corpus callosum (CC) is the largest of the brain commissures and consists of four parts; from anterior to posterior, these are the rostrum, genu, body, and splenium (1). The splenium (from Greek meaning “bandage” or “patch”) is the most dorsal and thickest part of the corpus callosum (CC) (2). Isolated splenium lesions are rare and have been associated with ischemic infarction, viral encephalitis, metabolic disorders, and drug and substance toxicity (3). They may present with altered consciousness, seizures, stupor, coma, headache, and psychiatric disorders (4).
Here, we present a case of a patient presenting to the emergency department with dizziness and a lesion in the corpus callosum splenium detected on diffusion-weighted MRI imaging.
CASE
A 20-year-old male patient presented with a complaint of dizziness persisting for 4 days. The patient had a GCS (Glasgow Coma Scale) score of 15, stable vitals, no fever, and normal fingertip blood sugar levels. There was no neck stiffness. Upon physical examination, cerebellar tests were proficient, and there was no ataxia. Rectal examination was normal. His electrocardiogram showed a normal sinus rhythm. As the symptoms did not alleviate with symptomatic treatment, central imaging was requested. While the brain CT scan appeared normal (Image 1), diffusion-weighted MRI imaging (DWI) revealed restricted diffusion in the corpus callosum splenium, as evidenced by corresponding findings on the apparent diffusion coefficient (ADC) sequence (Images 2 and 3). Further inquiry into the patient’s history revealed no substance use other than smoking, no intake of medication, or herbal supplements. It was learned that the patient had presented to the emergency department with similar complaints 5 months ago and was discharged upon normal DWI at that time. There were no abnormal values detected in the patient’s blood tests. The patient was referred to the Neurology department for consultation. The patient was admitted to the neurology ward for further monitoring and management.
Image 1. Normal Brain CT scan of the patient.
Image 2. Diffusion restriction on DWI.
Image 3. ADC image.
DISCUSSION
The splenium connects the occipital, parietal, inferior, and medial temporal cortex regions (5). Various neurological disorders are associated with lesions affecting specifically or primarily the splenium of the corpus callosum. These disorders include Marchiafava-Bignami syndrome (MBS), reversible splenial lesion (RSL), and ischemic stroke (IS) (1).
Focal imaging abnormalities of the corpus callosum are rare and have been described in various neurological disorders. Reversible splenial lesion (RSL) is not a common finding on MRI imaging and has been reported in only a few studies to date. The scarcity of RSL may be attributed to the use of different terminologies in the literature, such as MERS (mild encephalitis/encephalopathy with a reversible lesion in the splenium) or RESLES (reversible splenial lesion syndrome) (6).
The pathophysiology of reversible splenial lesion (RSL) is not yet well-defined. In its pathophysiology, intramyelinic axonal edema associated with hyponatremia and infiltration of local inflammatory cells are implicated (7).
Clinically, headache, nausea, vomiting, diarrhea, fever, dizziness, visual disturbances, and sensorimotor hemiparesis may be observed.
In the study by Foerster et al., the DWI image in our case (central oval or round lesion in the splenium) was associated with reversible splenial lesion (RSL). The median age of the diagnosed 10 patients in this study was 42 (IQR: 15-45), with 70% of the patients being male. Etiological factors identified included epileptic seizures, viral meningitis, hypoglycemia, septic abortion, hypernatremia, and carbamazepine withdrawal. Complete resolution was observed in all cases on follow-up MRI imaging (6).
In the study by Balcik et al., which included 16 cases, the average age was 52.3 years, with 11 of the patients being male. Complaints upon presentation included altered consciousness, headache, seizures, ataxia, hemiparesis, nonsensical speech, fever, perioral numbness, and diplopia. The identified etiologies included ischemic infarction, tuberculous meningitis, viral encephalitis, hypernatremia, brain tumor, Marchiafava-Bignami syndrome, head trauma, epilepsy, and substance use (1).
Although diffusion restriction typically reflects a vascular etiology, it can also be observed in many other neurological disorders such as seizures and status epilepticus. Additionally, it may occur in conditions including transient global amnesia, brain tumors, various etiologies of encephalopathies, and conditions like pontine and extrapontine myelinolysis (6).
DWI hyperintensity does not always indicate ischemic infarction. Decreased apparent diffusion coefficient (ADC) intensity reflects cytotoxic edema rather than neurological damage (4). Diffusion restriction observed in the splenium without ischemia is associated with cytotoxic mechanisms. This cytotoxic edema is typically transient; DWI abnormalities tend to resolve over time with removal of the pathological factor (1).
The prognosis is generally excellent. Conservative follow-up reveals complete resolution in nearly all lesions.
In conclusion, we know that the corpus callosum (CC) is a unique structure in terms of its vascular, cellular, and macroscopic characteristics, facilitating communication between the brain hemispheres. While radiological images of the splenium may suggest acute ischemic infarction, the actual cause could be another pathology. Various pathological events can lead to similar reversible focal lesions in the splenium. Therefore, the symptoms and etiology of splenium lesions should be considered and investigated in a broad context. In the presence of splenium lesions, non-ischemic metabolic causes should be considered before contemplating lytic therapy.
REFERENCES
1. Balcik ZE, Senadim S, Keskek A, Ozudogru A, Koksal A, Soysal A and Atakli D: Does restricted diffusion in the splenium indicate an acute infarct? Acta Neurol Belg 120(5): 1085-1089, 2020. PMID: 29307027. DOI: 10.1007/s13760-017-0876-6
2. Velut S, Destrieux C and Kakou M: [Morphologic anatomy of the corpus callosum]. Neurochirurgie 44(1 Suppl): 17-30, 1998. PMID: 9757322.
3. Oquist M, Farooq MU, Gorelick PB (2014) Restricted difusion of the splenium of the corpus callosum in viral meningitis. Neurohospitalist 4(2):109–110
4. Park MK, Hwang SH, Jung S, Hong SS, Kwon SB (2014) Lesions in the splenium of the corpus callosum: clinical and radiological implications. Neurol Asia 19(1):79–88
5. Putnam MC, Steven MS, Doron KW, Riggall AC and Gazzaniga MS: Cortical projection topography of the human splenium: hemispheric asymmetry and individual differences. J Cogn Neurosci 22(8): 1662-1669, 2010. PMID: 19583478. DOI: 10.1162/jocn.2009.21290
6. Foerster, A., Apfaltrer, P., Al-Zghloul, M., Wenz, H., Alonso, A., & Groden, C. (2022). Diffusion restricted lesions in the splenium of the Corpus Callosum. in vivo, 36(3), 1354-1359.
7. EREN, F., ÖNGÜN, G., & ÖZTÜRK, Ş. (2018). Clinical and Radiological Significance of Transient Brain Lesion in the Corpus Callosum Splenium: 2 Case Reports. Kafkas Journal of Medical Sciences, 8(2), 133-136.
