Possible presentation of Kernohan–Woltman notch phenomenon in a young female with heavy drinking: a case report

A subdural hematoma results from the rupture of bridging veins, most commonly from head trauma. It is a type of traumatic brain injury that can occur in people of all ages but is most common in older adults. The risk of developing a subdural hematoma increases with age, and it is more common in men than women. People who are at higher risk for subdural hematoma include those who have had a head injury, those who take anticoagulant medications, and those who have a history of alcohol abuse [1].

Intracranial pathology, including subdural hematoma, can lead to mass effect, which causes displacement and potential herniation of cerebral tissue. The pressure exerted by a mass effect can herniate a portion of the medial temporal lobe called the uncus medially against the ipsilateral midbrain. As a result, patients will present with contralateral hemiparesis, contralateral homonymous hemianopia, and ipsilateral mydriasis [2].

With severe pressure, a portion of uncus can displace the whole midbrain contralaterally and press the crus cerebri against the tentorial edge. Patients will present with a “false localizing sign” of ipsilateral hemiparesis, while the other symptoms will be the same. The process described is known as Kernohan–Woltman notch phenomenon (KWNP) [2].

This case reports a 30-year-old Caucasian female who presented to the emergency department with a decreased level of consciousness, left facial paresis, left hemiparesis, and diminished left pupillary light reflex. Imaging demonstrated a left subdural hematoma in the frontotemporoparietal region. The case is remarkable because the physical exam displayed paradoxical hemiparesis, ipsilateral to the subdural hematoma. The patient also demonstrated a delayed course of delirium tremens.

A 30-year-old female was brought in by emergency medical services due to altered mental status prior to admission. The patient’s partner reported that the patient had been binge drinking the previous night. The patient reported feeling weak and was unable to stand. The patient’s partner denied that the patient hit her head or experienced any loss of consciousness. The partner endorsed that the patient drank alcohol “heavily” but denied any drug use.

On primary survey, the patient’s Glasgow Coma Scale was rated to be 13 (E4, M6, V3) with inappropriate slurred speech and right-sided facial paresis. Eye examination revealed an attenuated left pupillary light reflex. There was weakness in the left upper and lower extremities (0/5), but the right upper and lower extremities had intact strength (5/5).

Laboratory analyses demonstrated a negative troponin (< 0.03 ng/mL) and an elevated blood alcohol level (318.5 mg/dL). There was evidence of thrombocytopenia with elevated poly-segmented neutrophils (94%). Computed tomography (CT) scan of the head without contrast revealed a left subdural hematoma (10 mm) with an associated midline shift to the right (6 mm) in the frontotemporoparietal region (Fig. 1). A left frontotemporoparietal craniotomy was indicated for evacuation. After evacuation, hemifacial paresis and ocular dysfunction resolved, however, left upper and lower extremity weakness persisted. The clinical course demonstrated resolution of the hematoma from 4.61 mm on postoperative day (POD) #2 to 3.9 mm on POD #16.

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Magnetic resonance angiography (MRA) of the head was performed on POD #2 to rule out acute ischemic stroke (Fig. 2). No significant stenosis or occlusion involving anterior or posterior intracranial circulation was noted. CT angiogram of the chest with and without contrast was also performed which was unremarkable. Echocardiogram on POD #2 showed an ejection fraction (EF) of 55 to 60% with ultrasound demonstrating < 50% stenosis of bilateral carotid arteries.

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Magnetic resonance imaging (MRI) of the brain on POD #2 revealed a signal in the contralateral midbrain on T1 axial scan, prompting suspicion of an alternate etiology of the paradoxical ipsilateral hemiparesis (Fig. 3).

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The patient’s clinical course remained remarkable for associations with alcohol withdrawal. On POD #2, the patient experienced a seizure where an electroencephalogram (EEG) demonstrated poorly organized theta waves (6–7 Hz), suggesting encephalopathy. Starting on POD #5, the patient displayed signs of aggression (e.g., pulling out their nasogastric tube). On POD #6, the patient was found to have elevated troponins (2.753 ng/mL) that were thought to have been secondary to a type II NSTEMI in the setting of a subdural hematoma. Another echocardiogram done on POD #8 found global systolic hypokinesis with EF between 35 to 40% with abnormal diastolic filling and mild mitral regurgitation, possibly due to alcoholic cardiomyopathy. By POD #35, the patient demonstrated 5/5 strength bilaterally in the upper and lower extremities with resolved cranial nerve dysfunctions.

In KWNP, compression of the contralateral cerebral peduncle in a subdural hematoma can damage the descending corticospinal tract and subsequently cause ipsilateral hemiparesis. There can be wide variability in the morphology of this pathology [3]. Thus, it is important to differentiate KWNP from other etiologies of ipsilateral hemiparesis like cerebrovascular dysfunction of the contralateral hemisphere or mass effect from cerebral neoplasms. Our postoperative studies did not provide clinical evidence in support of an ischemic stroke or malignancy.

KWNP is rarely reported in the literature especially in young women and in patients with heavy alcohol use. A systematic review of English-language articles containing KWNP found that the mean age of presentation was 40.7 years old and the male/female sex ratio was 2:1. Interestingly, in previous studies, the mechanism behind KWNP seemed to primarily arise from head trauma (e.g., blunt trauma, falls, car crashes, etc.) [4]. In our patient, the historian denied any trauma to the head and the physical exam did not reveal any contusions or evidence of trauma. Additionally, only one other study emerged that demonstrated KWNP in a patient with a history of alcohol abuse [5]. It has been well-documented that alcohol use is a risk factor for acute and chronic subdural hematoma [1, 6]. Further investigation into the link between chronic alcohol use and the presence of KWNP could be warranted in future studies.

Another incidental finding in our case report was the delayed emergence of delirium tremens. In our patient, the constellation of symptoms associated with delirium tremens (e.g., autonomic dysfunction, agitation, acute coronary syndrome) occurred on POD #6. Delirium tremens are typically seen between 48 and 96 h after a patient ceases ingestion of ethanol [7]. The phenomenon is already rare: about 50% of patients with alcohol use disorder will develop alcohol withdrawal syndrome and about 3% to 5% of those patients will develop delirium tremens [8]. Due to the short-acting nature of ethanol, withdrawal symptoms typically begin within 8 h after blood alcohol levels start to decrease. These symptoms peak at approximately 72 h. The symptoms tend to abate by 120 h [9, 10]. In our patient, the autonomic hyperactivity, psychomotor agitation, and coronary sequelae of delirium tremens started approximately at 144 h. This incidental finding was hypothesized to be due to the patient being extubated on POD #3. There is a lack of research documenting the time course of delirium tremens in patients who were intubated. Future studies and case reports may provide further insight into how intubation may delay the emergence of delirium tremens.

By ruling out cerebrovascular dysfunction, ischemic stroke, and structural abnormalities, our case report strengthens the differential diagnosis of KWNP in a patient with paradoxical ipsilateral hemiparesis. This report also contributes to the existing literature that associates subdural hematomas with KWNP. Our presentation provides an uncommon demographic of KWNP (e.g., a young woman) in the setting of chronic alcohol use with severe complications. It is worth noting that we did not obtain ancillary studies such as coronal views of the MRI, diffusion tensor imaging, or motor-evoked potentials. These have previously been reported to visualize KWNP in the literature [11].

Additionally, our report illustrates a case of late delirium tremens. Given the significant morbidity linked with delirium tremens and its varied presentation, this report could guide future diagnostic protocols for identifying delirium tremens. Subsequent research could explore the underlying pathophysiology contributing to the delay in the onset of delirium tremens, potentially attributed to intubation.

This case underscores the importance of considering KWNP in cases of paradoxical ipsilateral hemiparesis associated with subdural hematomas, especially in young individuals with heavy alcohol use. Early detection of KWNP could lead to refined diagnostic algorithms and advance our understanding of this rare phenomenon. The case report provides an alternative method to rule out other possible etiologies of ipsilateral hemiparesis through imaging studies when characteristic features of the disease are not easily located. Further research is needed to uncover its underlying mechanisms and risk factors.

Our case demonstrates the heterogeneity in the spectrum of presentations of KWNP as well as delirium tremens. Specifically, we present the paradoxical ipsilateral hemiparesis associated with KWNP in an underreported demographic. Additionally, we explored an incidental finding of delayed delirium tremens possibly due to intubation. Our case provides insight into these uncommon neurological and psychiatric phenomena that may inform enhanced diagnostic algorithms. Future research may investigate the temporal aspect of the onset of delirium tremens. Studies in the future may also examine the underlying risk factors, early diagnosis, and pathophysiology of KWNP. Our case report contributes to future studies on KWNP and delirium tremens by providing helpful information on uncommon presentations for researchers and clinicians.