Beyond uncal herniation: An updated diagnostic reappraisal of ipsilateral hemiparesis and the Kernohan-Woltman notch phenomenon.

PURPOSE: This works comprehensively analyses a modern cohort of patients with ipsilateral hemiparesis (IH) and discusses the pathophysiological theories elaborated to explain this paradoxical neurological sign according to the findings from contemporary neuroimaging and neurophysiological techniques. METHODS: A descriptive analysis of the epidemiological, clinical, neuroradiological, neurophysiological, and outcome data in a series of 102 case reports of IH published on since the introduction of CT/MRI diagnostic methods (years 1977-2021) was performed. RESULTS: IH mostly developed acutely (75.8%) after traumatic brain injury (50%), as a consequence of the encephalic distortions exerted by an intracranial haemorrhage eventually causing contralateral peduncle compression. Sixty-one patients developed a structural lesion involving the contralateral cerebral peduncle (SLCP) demonstrated by modern imaging tools. This SLCP showed certain variability in its morphology and topography, but it seems pathologically consistent with the lesion originally described in 1929 by Kernohan & Woltman. The study of motor evoked potentials was seldom employed for the diagnosis of IH. Most patients underwent surgical decompression, and a 69.1% experienced some improvement of the motor deficit. CONCLUSIONS: Modern diagnostic methods support that most cases in the present series developed IH following the KWNP model. The SLCP is presumably the consequence of either compression or contusion of the cerebral peduncle against the tentorial border, although focal arterial ischemia may also play a contributing role. Some improvement of the motor deficit should be expected even in the presence of a SLCP, provided the axons of the CST were not completely severed.

Temporal lobe uncal herniation with contralateral superior cerebellar artery infarct.

Herniation of the temporal lobe uncus typically leads to the compression of the ipsilateral oculomotor nerve, resulting in ipsilateral mydriasis, as well as compression of the ipsilateral posterior cerebral artery, leading to infarction in the posterior inferior temporal lobe and medial occipital cortex. In this report, we present the case of a 45-year-old man with a large left subdural hematoma. At autopsy, we observed left cingulate and uncal herniations, along with the characteristic lesions of Kernohan notch phenomenon due to compression of the contralateral cerebral peduncle. Additionally, a hemorrhagic infarct was identified in the right cerebellar hemisphere in the distribution of the superior cerebellar artery (SCA). This case provides the first autopsy report of uncal herniation with contralateral SCA infarct, an extremely rare condition. Importantly, this vascular complication may often go unnoticed in patients with Kernohan notch phenomenon although it may carry a grave clinical prognosis.

Midline Shift Induced by the Drainage of Cerebrospinal Fluid in Three Patients With External Decompression.

It is not rare that progressive hydrocephalus worsens clinical conditions in a patient with external decompression and drainage or shunt surgery is required. However, spinal drainage or shunt surgeries potentially carry a risk of causing paradoxical herniation in a patient with decompressive craniectomy, particularly in a comatose case with wide craniectomy. Careful and strict observations are necessary for such patients. In our three comatose cases with craniectomy, paradoxical herniation occurred due to excessive drainage after 5-7 days of shunt surgery and lumbar drainage, although the drainage pressure was set at more than 10 cmH2O. Fortunately, in the three cases, the herniation improved within a few days after the drain was clamped and the bed was flattened. However, the Trendelenburg position and epidural blood patch might be necessary if paradoxical herniation occurs acutely after lumbar puncture or drainage because delayed resolution can be fatal in the herniation.

Spontaneous intracranial hypotension complicated by unilateral subdural hematoma, coma, and the rare Kernohan's notch phenomenon.

Spontaneous intracranial hypotension (SIH) is a highly underdiagnosed condition with a wide range of manifestations. Although SIH has traditionally been viewed as having a benign disease course, recent evidence suggests otherwise. In this case report, we present a 71-year-old woman who was previously treated with a tapered dose of corticosteroids for an episode of SIH with behavioral manifestations. In this current report, we present her second episode which was complicated by a unilateral sub-acute subdural hematoma leading to loss of consciousness and coma. While the patient regained full consciousness and recovered considerably, she still suffers from ipsilateral hemiparesis as a result of Kernohan's notch phenomenon 2 years post-hospitalization. To the author's knowledge, this is the first case to involve persistent motor deficit after the resolution of SIH. We believe that surgical hematoma evacuation prior to addressing the cerebrospinal fluid leak may have contributed to aggregated downward displacement of the brain precipitating Kernohan's notch phenomenon.

Kernohan-Woltman notch phenomenon: an exceptional neurological picture?

INTRODUCTION: Ipsilateral hemiparesis (IH) can be defined as a paradoxical dysfunction of the first motor neuron involving the extremities on the opposite side to that expected, given the location of the triggering intracranial pathology. Compression of the corticospinal tract (CSt) along its course through the contralateral cerebral peduncle against the free edge of the tentorium, known as the Kernohan-Woltman notch phenomenon (KWNP), represents the main cause of IH. METHODS: This retrospective study analyses a series of 12 patients diagnosed with IH secondary to KWNP treated at our institution, including a descriptive study of epidemiological, clinical, radiological, neurophysiological, and prognostic variables. RESULTS: In 75% of the cases, symptoms had an acute or subacute onset. Initial imaging studies showed signs of significant mass effect in half of the patients, whereas magnetic resonance imaging (MRI) identified a structural lesion in the contralateral cerebral peduncle in two thirds of them. Impairment of the motor evoked potentials (MEP) was verified in 4 patients. During follow-up 7 patients experienced improvement in motor activity, and near half of the cases were classified in the first three categories of the modified Rankin scale. CONCLUSIONS: In contrast to prior historical series, most of our patients developed a KWNP secondary to a traumatic mechanism. MRI represents the optimal method to identify both the classic cerebral peduncle notch and the underlying structural lesion of the CSt. The use of MEP can help to establish the diagnosis, especially in those cases lacking definite radiological findings.

Delayed Hemiparkinsonism Associated with Kernohan's Notch in a Patient with a Ruptured Arteriovenous Malformation.

A 24-year-old female patient was admitted for a right frontal intracranial hematoma with an uncal herniation due to a ruptured arteriovenous malformation and therefore underwent emergency surgery. Neuroimaging revealed left-sided midbrain notching against the tentorium, indicating Kernohan's notch phenomenon. She denied experiencing any short-term neurological deficits but right-sided delayed hemiparkinsonism developed 18 months later. Dopamine transporter tracer uptake was severely reduced in the left striatum, suggesting nigrostriatal degeneration secondary to Kernohan's notch. Uncal herniations are potentially fatal, but surgery can save the patient's life and improve the functional outcomes. Clinicians should therefore be aware of delayed hemiparkinsonism as a rare complication of Kernohan's notch phenomenon.

Automated Pupillometry and Detection of Clinical Transtentorial Brain Herniation: A Case Series.

Introduction: Transtentorial herniation (TTH) is a life-threatening neurologic condition that typically results from expansion of supratentorial mass lesions. A change in bedside pupillary examination is central to the clinical diagnosis of TTH. Materials and. Methods: To quantify the changes in the pupillary examination that precede and accompany TTH and its treatment, we evaluated 12 episodes of herniation in three patients with supratentorial mass lesions using automated pupillometry (NeurOptics, Inc., Irvine, CA). Herniation was defined clinically by the onset of fixed and dilated pupils in association with decreased levels of consciousness. Automated pupillometry was measured simultaneously with the bedside clinical examination, but the clinical team was blinded to these results and could not act on the data. Data from the pupillometer were downloaded 1-2 times per week onto a secured laptop, and data processing was facilitated by the use of Mathematica 8.0. Results: Neurologic Pupil Index measurements, values generated by the pupillometer based on an algorithm that incorporates pupillary size and reactivity in a normal population, were found to be abnormal before 73% of TTHs. This abnormality occurred at a median of 7.4 h before TTH. All episodes of TTH were reversed after clinical intervention at a median of 43 min after the event. The value did not fall to 0 in 42% of clinical herniations, but it did decrease to very abnormal values of 0.5-0.8. Conclusions: The potential of automated pupillometry to guide the management of severely injured neurologic patients is intriguing and warrants further study in the critical care unit and beyond. The utility of a portable device in the combat setting may allow for triage of patients with severe neurologic injury.