INTERMITTENT MEMORY LOSS, DIPLOPIA, SPARKLING LIGHTS, AND…

Question Answered step-by-step INTERMITTENT MEMORY LOSS, DIPLOPIA, SPARKLING LIGHTS, AND… INTERMITTENT MEMORY LOSS, DIPLOPIA, SPARKLING LIGHTS, AND SOMNOLENCE A 60-year-old retired businesswoman was sent to the emergency room by her physician because of 2 months of worsening episodes of memory loss, sparkling lights, and blurry or double vision. Her past medical history was notable for anticardiolipin (antiphospholipin) antibody syndrome (a condition causing hypercoagulability; see Table 10.5), including elevated anticardiolipin antibodies (IgG 2407, IgM 38, IgA < 10), a first-trimester miscarriage, left subclavian stenosis, and Raynaud's phenomenon. She had been treated in the past with Coumadin, but she elected to take aspirin instead. She also had a long history of brief, 1- to 2-minute, episodes of migrainelike visual scintillations (see KCC 5.1) that she described as "like firecrackers going off in front of my eyes," associated with multiple other vague complaints, including epigastric, pleuritic, and back pain, which were attributed to fibromyalgia or stress. There was a strong family history of migraine. The patient's sister had died 2 months prior to admission, and shortly afterward the patient began having recurrent episodes of memory loss lasting several minutes each, along with worsening of all her other complaints. She was somewhat evasive and vague in describing the episodes, and her physicians initially believed them to be psychiatrically based. Memory lapses included forgetting whether her sister had been buried or cremated and forgetting a real estate deal she had recently completed. On the day of admission, she saw her physician because of a new complaint she had developed a few days earlier of blurred and then double vision to the point where it was difficult for her to stand up and walk. On initial examination she was alert and fluent but had mildly reduced attention, able to repeat only 5/7 digits forward, and recalling 2/3 objects after 3 minutes. Her right pupil was slightly enlarged at 4 mm, constricting sluggishly to 2.5 mm, and her left pupil was 3 mm, constricting briskly to 2 mm. She had limited upward gaze with both eyes. In addition, medial gaze was reduced with the right eye, and she had a right ptosis. Exam was otherwise unremarkable. Her physician sent her to the emergency room, where she was examined by a neurologist, but by the time she arrived she had normal eye movements, with the only abnormality on exam being a mild residual anisocoria. She was admitted for further evaluation, and the next morning she was found again to have limited upgaze bilaterally, right ptosis, and right limited medial gaze, with a somewhat dilated right pupil. Anticoagulation with intravenous heparin was initiated; however, during the subsequent days she had waxing and waning somnolence and delirium to the point of being unarousable at times. At other times, despite being transferred to the intensive care unit, she would wake up, pull out all her intravenous lines, and walk down the hallway to use the bathroom. Her eye movement abnormalities persisted, and in addition she developed bilateral ataxia on finger-to-nose testing (when she was awake enough to cooperate) and decreased blink to visual threat on the left side.The key symptoms and signs in this case are: • Episodes of memory loss • Mildly reduced attention evolving to waxing and waning somnolence and delirium • Limited upward gaze with both eyes • Double vision with limited right medial and upward gaze, enlarged right pupil, and right ptosis • Bilateral ataxia on finger-to-nose testing • Sparkling lights, blurry vision, and, later, decreased blink to visual threat on the left side 1. Summary of eye movement abnormalities: The patient had limited upgaze bilaterally. In addition, she had findings compatible with right third-nerve dysfunction, including right ptosis, a large right pupil with decreased reactivity to light, and reduced right eye adduction in addition to the limited upgaze. 2. Localization of eye movement abnormalities, somnolence, and ataxia: Dysfunction in the midbrain tegmentum could cause (1) vertical gaze abnormalities through involvement of the rostral interstitial nucleus of the MLF in the rostral midbrain (2) right third-nerve dysfunction through involvement of the right third nerve fascicles or nucleus (a right third-nerve nucleus lesion involving the ipsilateral superior rectus subnucleus, and contralateral crossing fibers, could also cause bilateral impairment of upgaze; (3) somnolence and delirium through involvement of the reticular formation and (4) bilateral ataxia through involvement of the superior cerebellar peduncle fibers. Vascular localization and diagnosis: Given this patient's history of hypercoagulability, a thromboembolic disorder is likely. The above deficits can be localized to the midbrain tegmentum, which is supplied by small penetrating vessels arising from the top of the basilar artery and proximal PCAs (see Figure 14.18A, Figure 14.20, and Figure 14.21A). The left visual field deficit could be explained by an infarct of the right occipital lobe, which is supplied by the right PCA. In addition, the episodes of memory loss could have been caused by TIAs involving the bilateral medial thalami or medial temporal lobes , and these structures are also supplied by the PCAs . Therefore, the above deficits could all be caused by vascular insufficiency at the top of the basilar artery and proximal PCAs, known as top-of-the-basilar sydrome . Top-of-the-basilar syndrome is usually caused by an embolus or thrombus lodged at the top of the basilar artery. Another, less likely possibility is thrombosis of the more proximal basilar artery, although in that case pontine dysfunction usually occurs, including corticospinal, horizontal gaze, proprioceptive, and other dysfunctions not seen in this patient. As already noted, despite anticoagulation the patient's condition continued to wax and wane. MRI and head CT scans demonstrated multiple bilateral infarcts in the territory of vessels arising from the top of the basilar artery , including the midbrain tegmentum, bilateral medial thalami, and right occipital lobe. An angiogram was performed because of concerns that, given her rheumatological history, she might have CNS vasculitis (see Table 10.5) which would require a different treatment (immunosuppressive therapy). The angiogram was negative for changes suggestive of vasculitis. However, a filling defect was seen at the top of the basilar artery, most likely due to a thrombus that had embolized to that location from a remote source such as the heart or, less likely, due to a thrombus that had formed locally. Of note, the PCAs did not fill from the basilar artery. However, when the internal carotid arteries were injected , the PCAs did fill, via the posterior communicating arteries, except for the distal right PCA. This result suggests that the midbrain and thalamic infarcts were caused by the occlusion of small penetrating vessels arising from the top of the basilar artery and proximal PCAs , while the right occipital infarct was probably caused by an embolus that broke off from the top of the basilar region and migrated up into the distal right PCA . During the course of her hospital stay, the patient's condition initially waxed and waned, as already noted, but she later developed right hemiplegia and lapsed into a coma . A week later, she began to regain some responsiveness to stimulation and to commands, and an MRA revealed that some flow had been restored through the distal basilar artery. She was eventually discharged on Coumadin to a rehabilitation facility.Based on the reading from the above mentioned clinical case from the book Neuroanatomy through clinical cases by Blumenfeld second edition. chapter 14 Please answer the following questionwhat is History:AssessmentsDiagnostic TestingArriving at a diagnosis with differential diagnosisApproaches to treatmentIs there in excess that you would consider in your assessments? Are there any treatments that you would consider in excess?Please include references ---online medical sitesThank you Health Science Science Nursing NURS 598 Share QuestionEmailCopy link Comments (0)