Heralding manifestations of basilar artery occlusion with lethal or severe stroke

Abstract

Background: Basilar artery occlusion usually causes severe disability or death. Until the recent developments in local intra-arterial or systemic intravenous fibrinolysis, interest in early diagnosis was low because there was no satisfactory treatment. Thus there is little information about the initial phase of the disease. Objective: To report on the early clinical features and patterns of evolution of severe symptomatic basilar artery occlusion. Methods: 24 patients with established basilar artery occlusion (confirmed by angiography or at necropsy) were reviewed retrospectively, focusing on the early clinical aspects and time course of the disease. Results: The most common initial symptoms were motor deficits (16/24, including facial palsies), articulatory speech difficulties (15/24), vertigo, nausea or vomiting (13/24), and headaches (10/24). The most frequent objective initial findings were motor deficits (22/24), facial palsies (19/24), eye movement abnormalities (15/24), lower cranial nerve deficits (15/24), altered level of consciousness (12/24), and bilateral extensor plantar responses (9/24). Onset of the disease was gradual in nearly all patients and in half the warning signs were present for up to two months before the final stage. Headaches and visual disturbances were early signs, while speech difficulties and motor deficits were late signs. Once permanent neurological deficits were present, the final illness was reached within six hours in 41%, between six and 24 hours in 32%, and in two to three days in 27%. Conclusions: All the patients reviewed presented some symptoms and signs pointing to brain stem involvement. Only 8% (2/24) had an acute course with no adequate warning signs.

Posterior circulation ischaemic stroke

“…Basilar migraine, which may have aura features including vertigo and diplopia, as well as severe occipital headache, can resemble acute stroke, and should always be excluded, especially if it is the patient's first presentation. 21 Toxic or metabolic disturbances may initially present with features resembling cerebrovascular disease. These include drugs of misuse or prescribed drugs (such as anticonvulsants), hypoglycaemia, central pontine myelinolysis, and post-infectious disorders, such as antibody associated disorders (for example, Miller Fisher syndrome, which causes ophthalmoplegia, ataxia, and areflexia).…”

“…These include drugs of misuse or prescribed drugs (such as anticonvulsants), hypoglycaemia, central pontine myelinolysis, and post-infectious disorders, such as antibody associated disorders (for example, Miller Fisher syndrome, which causes ophthalmoplegia, ataxia, and areflexia). 21 Posterior reversible encephalopathy syndrome can cause posterior circulation ischaemia, which results in visual disturbance, seizures, and other focal symptoms. This syndrome …”

“…21 Between 55% and 63% of patients with basilar artery occlusion have prodromal TIAs, minor strokes, or other symptoms, which are more common with atherosclerotic than embolic occlusions. 22 Patients with acute basilar artery occlusion have high mortality rates of 41-95% in natural history studies or studies of intravenous thrombolysis, with mortality rates being highest when there is no recanalisation.…”

Neurological Complications and Aspects of Basilar Artery Occlusive Disease

“…Motor symptoms without sensory symptoms are a hallmark of proximal brain stem infarcts. 18 However, PCA artery infarctions can present with sensory symptoms in 25% of cases, as shown by Alexandros et al 21 Uson-Martin and Gracia-Naya 19 observed the most common clinical manifestation of BAO to be motor deficit (68%). Added manifestations included abnormal eye movements (48%), cerebellar …”

Patterns and Outcomes of the Top of the Basilar Artery Syndrome: The Role of the Posterior Communicating Artery

“…In these patients, downward extension of the thrombus occludes the pontine perforators, resulting in extensive ischemic damage to the areas below the distal BA [23], without effective collateral flow through the PcoA. These patients generally show progressive worsening of neurological outcome even if their initial symptoms are mild as described by von Campe et al [24] Therefore, the patterns and clinical outcomes of patients with TOB are affected by the presence or type of the PcoA, as well as recanalization of the BA associated with characteristics (e.g., size or fragility) of the thrombus. Moreover, as in patients with anterior circulation infarct [25], early reperfusion therapy was associated with favorable 1-year mortality.…”