A Rare Case Report of Eight Syndrome Secondary to Syringomyelia Associated with Type I Chiari Malformation.

Eight syndrome is defined as the combination of a unilateral conjugate gaze palsy and ipsilateral seventh cranial nerve palsy. It may occur as a result of demyelinating, vascular, infectious, or compressive lesions of the brainstem localized to the caudal pontine tegmentum. A 43-year-old woman was admitted to our clinic with complaints of headache, inability to look to the left, and weakness on the left side of her face. The complaints had begun abruptly about a month before her admission. Suboccipital decompression surgery for type I Chiari malformation had been performed 10 years earlier. Neuro-ophthalmological examination revealed left-sided horizontal gaze palsy and anisocoria. Cranial and cervical magnetic resonance images revealed cerebellar tonsillar herniation and syringomyelia, the latter of which was considered to be the cause of eight syndrome. No interventions were performed, and periodic follow-up was advised on neurosurgical consultation. Left gaze palsy and facial palsy recovered almost completely in three months, while the anisocoria persisted. Syringomyelia should be considered among the causes of horizontal gaze palsy plus ipsilateral seventh nerve palsy, termed as eight syndrome. Clinical suspicion and appropriate radiological examination can aid in the diagnosis.

Hemiplegia resulting from acute carbon monoxide poisoning.

Carbon monoxide (CO) poisoning can cause neurological complications such as movement disorders and cognitive impairment through hypoxic brain damage. Although peripheral neuropathy of the lower extremities is a known complication of CO poisoning, hemiplegia is very rare. In our case, a patient who developed left hemiplegia due to acute CO poisoning received early hyperbaric oxygen treatment (HBOT). The patient had left hemiplegia and anisocoria at the beginning of HBOT. Her Glasgow coma score was 8. A total of five sessions of HBOT at 243.2 kPa for 120 minutes were provided. At the end of the 5th session, the patient's hemiplegia and anisocoria were completely resolved. Her Glasgow coma score was 15. After nine months of follow-up, she continues to live independently with no sequelae, including delayed neurological sequelae. Clinicians should be aware that CO poisoning can (rarely) present with hemiplegia.

[Painful anisocoria in a five-year-old child: A rare diagnosis which must not be missed]. / Anisocorie douloureuse chez un enfant de cinq ans : un diagnostic rare à ne pas méconnaître.

Congenital ectropion uveae (CEU) is a rare anomaly of the embryonic development of the anterior segment of the eye. We report the case of a 5-year-old child with an undiagnosed CEU who was treated urgently for an acute angle closure attack. CASE DESCRIPTION: A 5-year-old child was referred urgently for evaluation of anisocoria with mydriasis of the right eye and severe headache. Brain imaging with contrast injection was initially performed in the pediatric emergency department and ruled out central nervous system pathology. The initial examination of the right eye revealed an intraocular pressure (IOP) of 37mmHg, corneal edema, congenital ectropion uveae, mydriasis with pupillary block, a closed angle on gonioscopy, and a clear lens. The examination of the left eye was unremarkable, with no visible CEU. The initial management consisted of medical treatment with topical glaucoma drops and miotics and acetazolamide at 10mg/kg/d. Re-evaluation under general anesthesia showed persistent mydriasis and no resolution of the pupillary block. Filtering surgery was performed in the absence of a complete response to medical treatment, allowing control of IOP without drops and complete regression of the corneal edema. DISCUSSION: CEU is a rare malformation, and pressure complications represent an insignificant proportion of pediatric glaucoma cases. The acute presentation of acute angle closure in this potentially blinding short-term setting, however, makes detection and management difficult in very young children in a great deal of pain. Only one similar case has been reported in the pediatric literature. CONCLUSION: Acute angle closure complicating CEU is exceptional and difficult to diagnose in a pediatric context. Parents of children with this predisposing condition should be informed of the need to consult urgently when clinical signs of elevated intraocular pressure appear.

Anisocoria and mydriasis after scalp nerve block: a case report.

Strategies for the assessment of abnormal neurological findings during general anesthesia are limited. However, pupil abnormalities may represent serious neurological complications. We herein present a case of new-onset anisocoria and mydriasis that developed after scalp nerve block. The patient's signs were possibly related to increased intracranial pressure with resulting brain shift that ultimately affected the oculomotor nerves. A 45-year-old man was scheduled for left cerebellar tumor resection and ventricular drainage surgery; however, anisocoria and left pupillary mydriasis were observed after induction of general anesthesia and performance of scalp nerve block. After reducing the intracranial pressure, the right pupil showed constriction (1 mm) but the left pupil was dilated (5 mm). The pupils were of similar size postoperatively. Although pupillary dilation during general anesthesia has been previously described, this is the first case in which the mydriasis was considered to have been caused by brain shift due to increased intracranial pressure after scalp nerve block. Thus, we propose this phenomenon as a new possible cause of pupillary changes. Actively monitoring this presentation intraoperatively could enable early detection of and intervention for complications, therefore improving the prognosis.

Anisocoria and Poor Pupil Reactivity by Quantitative Pupillometry in Patients With Intracranial Pathology.

OBJECTIVES: To describe the prevalence and associated risk factors of new onset anisocoria (new pupil size difference of at least 1 mm) and its subtypes: new onset anisocoria accompanied by abnormal and normal pupil reactivities in patients with acute neurologic injuries. DESIGN: We tested the association of patients who experienced new onset anisocoria subtypes with degree of midline shift using linear regression. We further explored differences between quantitative pupil characteristics associated with first-time new onset anisocoria and nonnew onset anisocoria at preceding observations using mixed effects logistic regression, adjusting for possible confounders. SETTING: All quantitative pupil observations were collected at two neuro-ICUs by nursing staff as standard of care. PATIENTS: We conducted a retrospective two-center study of adult patients with intracranial pathology in the ICU with at least a 24-hour stay and three or more quantitative pupil measurements between 2016 and 2018. MEASUREMENTS AND MAIN RESULTS: We studied 221 patients (mean age 58, 41% women). Sixty-three percent experienced new onset anisocoria. New onset anisocoria accompanied by objective evidence of abnormal pupil reactivity occurring at any point during hospitalization was significantly associated with maximum midline shift (ß = 2.27 per mm; p = 0.01). The occurrence of new onset anisocoria accompanied by objective evidence of normal pupil reactivity was inversely associated with death (odds ratio, 0.34; 95% CI, 0.16-0.71; p = 0.01) in adjusted analyses. Subclinical continuous pupil size difference distinguished first-time new onset anisocoria from nonnew onset anisocoria in up to four preceding pupil observations (or up to 8 hr prior). Minimum pupil reactivity between eyes also distinguished new onset anisocoria accompanied by objective evidence of abnormal pupil reactivity from new onset anisocoria accompanied by objective evidence of normal pupil reactivity prior to first-time new onset anisocoria occurrence. CONCLUSIONS: New onset anisocoria occurs in over 60% of patients with neurologic emergencies. Pupil reactivity may be an important distinguishing characteristic of clinically relevant new onset anisocoria phenotypes. New onset anisocoria accompanied by objective evidence of abnormal pupil reactivity was associated with midline shift, and new onset anisocoria accompanied by objective evidence of normal pupil reactivity had an inverse relationship with death. Distinct quantitative pupil characteristics precede new onset anisocoria occurrence and may allow for earlier prediction of neurologic decline. Further work is needed to determine whether quantitative pupillometry sensitively/specifically predicts clinically relevant anisocoria, enabling possible earlier treatments.

Isolated Anisocoria as a Presenting Stroke Code Symptom is Unlikely to Result in Alteplase Administration.

BACKGROUND: Acute stroke codes may be activated for anisocoria, but how often these codes lead to a final stroke diagnosis or alteplase treatment is unknown. The purpose of this study was to assess the frequency of anisocoria in stroke codes that ultimately resulted in alteplase administration. METHODS: We retrospectively assessed consecutive alteplase-treated patients from a prospectively-collected stroke registry between February 2015 and July 2018. Based on the stroke code exam, patients were categorized as having isolated anisocoria [A+(only)], anisocoria with other findings [A+(other)], or no anisocoria [A-]. Baseline demographics, stroke severity, alteplase time metrics, and outcomes were also collected. RESULTS: Ninety-six patients received alteplase during the study period. Of the 94 who met inclusion criteria, there were 0 cases of A+(only). There were 9 cases of A+(other) (9.6%). A+(other) exhibited higher baseline National Institutes of Health (NIH) Stroke Scale scores compared to A- (17 versus 7; P = .0003), and no additional differences in demographics or alteplase time metrics. Final stroke diagnosis and other outcome measures were no different between A+(other) and A-. Of the A+ patients without pre-existing anisocoria, 5 of 6 (83%) had posterior circulation events or diffuse subarachnoid hemorrhage. CONCLUSIONS: In this exploratory analysis, zero patients with isolated anisocoria received alteplase treatment. Anisocoria as a part of the neurologic presentation occurred in 10% of alteplase patients, and was strongly associated with a posterior circulation event. Therefore, we conclude that anisocoria has a higher likelihood of leading to alteplase treatment when identified in the presence of other neurologic deficits.

Anisocoria secondary to inadvertent contact with scopolamine patch.

A unilaterally fixed mydriasis, also known as a 'blown pupil,' is considered an ominous sign concerning for intracranial pathology. Causes of anisocoria can range from benign to immediately life-threatening. When a patient presents with anisocoria, the concern for a fatal diagnosis leads the clinician to obtain numerous tests, many of which may be unnecessary. The authors present a case of a healthy woman in her 30s who presented with an acute unilateral mydriasis likely secondary to inadvertent contact with a scopolamine patch. On examination, she had no other neurological deficits. Further investigation did not reveal any abnormality. In the event of a patient with an isolated mydriasis in an otherwise healthy and conversant patient with no other neurological deficits, it is essential to rule out other causes before pursuing aggressive and unnecessary testing and treatment.

Neuro-Ophthalmology in Emergency Medicine.

Understanding the anatomy and physiology of the eye, the orbit, and the central connections is key to understanding neuro-ophthalmologic emergencies. Anisocoria is an important sign that requires a systematic approach to avoid misdiagnosis of serious conditions, including carotid dissection (miosis) and aneurysmal third nerve palsy (mydriasis). Ptosis may be a sign of either Horner syndrome or third nerve palsy. An explanation should be pursued for diplopia since the differential diagnosis ranges from the trivial to life-threatening causes.

The role of the physical examination in the evaluation of headache.

The population of patients suffering with headaches is vast and underserved. The most critical element in headache evaluation is the history. The targeted history not only differentiates primary from secondary headaches but also provides a realistic list of conditions associated with secondary headache. Several of these conditions do present with specific physical findings, such as papilledema, Horner's syndrome, or CN palsy. The targeted physical examination of the patient with headache takes less than 3 minutes. The ability simply to recognize but a few straightforward clinical findings directs the evaluation in the proper direction. If you enjoy seeing patients, feel competent identifying but a few physical findings, and understand the basics of primary and secondary headaches and facial pain, there is urgent need of your services.

[Effective factors in the outcome of head injury]. / Kafa yaralanmalarinda sonucu belirleyen etkenler.

BACKGROUND: In this study, the data that could be obtained from our patient record system were investigated with respect to factors affecting the outcome in adult patients with head injury. METHODS: The records of 356 adult head-injury patients (308 males, 48 females; mean age 43.1 +/- 18.6 years; range 17 to 87 years) hospitalized in Trakya University Hospital, Department of Neurosurgery and the Intensive Care Unit were examined. Results of the obtained data were analyzed statistically. RESULTS: Age (p = 0.012), use of airway tube (p < 0.001), Glasgow Coma Scale values determined at the injury site and in the Emergency Unit (p < 0.001), clustered systolic and diastolic tricuspid annulus values (p < 0.001), accompanying chest (p = 0.001) and abdominal (p = 0.041) injury, anisocoria (p = 0.001), pupillary light response (p < 0.001), intracranial radiologic findings such as subdural hematoma (p < 0.001), brain contusion (p = 0.006), traumatic subarachnoid hemorrhage (p < 0.001), traumatic intracranial hemorrhage (p = 0.005), and brain edema ( p < 0.001), performance of a surgical procedure (p < 0.001), and presence of nosocomial infection (p < 0.001) were demonstrated to cause significant differences in the outcome. CONCLUSION The main aim must be to reduce accidents in an effort to reduce the number of deaths due to head injuries; additionally, emergency and hospital care facilities should be developed with respect to head injury cases.

Effect of anesthesia in a patient with pre-existing anisocoria.

In this case report, we describe an accentuation of a pre-existing anisocoria shortly after tracheal intubation in a patient undergoing thyroidectomy. A 45-yr-old female patient with unequal pupillary diameter (right 2 mm > than left) and decreased light reflex in the right eye--due to a previous eye trauma--was scheduled for thyroidectomy because of multinodular goiter. Anesthesia was induced with propofol 2,5 mg/kg, fentanyl 3 mcg/kg and cisatracurium 0.15 mcg/kg. Immediately after tracheal intubation, examination of the right eye revealed a markedly dilated pupil (8 mm) which was nonreactive to direct and consensual light reflex. The left pupil was 2 mm, and normally reactive to light. An increase in heart rate was also registered (> 20% of baseline) with spontaneous return to baseline within 2 minutes. The right pupil returned to preoperative size within approximately one hour after awakening. From this case report, it emerges that a preexisting anisocoria may be exacerbated during anesthesia probably due to incomplete abolition of response to painful stimulus, such as tracheal intubation, provided by anesthetic drugs in the affected eye. The main contributing factor for accentuation of anisocoria could be sympathetic dominance in the pupil with pre-existing mechanical interruption in compensatory parasympathetic mechanisms.

Oculosympathetic hyperactivity in idiopathic hyperhidrosis.

We describe a patient suffering from idiopathic hyperhidrosis, more pronounced on the right side, who presented with intermittent oculosympathetic hyperactivity (mydriasis, lid retraction and more rapid pupillary dilatation) on the same side. Mydriasis was induced by stress, loss of sleep and cold pressor test. The clinical features in this patient suggest an involvement of the hypothalamic structures.

Unilateral hyperhydrosis in Pourfour du Petit syndrome.

Upper limp hyperhydrosis is an idiopathic disease with bilateral involvement. However, Pourfour du Petit syndrome, the opposite of Horner syndrome, may result in unilateral upper limb hyperhydrosis. It occurs following hyperactivity of the sympathetic cervical chain as a consequence of irritation secondary to trauma. We report herein two cases with Pourfour du Petit syndrome showing unilateral upper limb hyperhydrosis. The patients presented with right-sided mydriasis and ipsilateral hemifacial hyperhydrosis. The onset of disease was followed by a trauma in both patients. They underwent upper thoracic sympathectomy with favorable outcome. A history of an antecedent trauma in patients with unilateral upper limb hyperhydrosis and anisocoria may imply a possible diagnosis of Pourfour du Petit syndrome.

Anisocoria and middle cerebral artery saccular (berry) aneurysm in a rhesus macaque (Macaca mulatta).

A 27-year-old female rhesus macaque (Macaca mulatta) developed anisocoria. The left pupil was dilated and unresponsive to light. The macaque was euthanized because of unrelated reasons and the body was submitted for necropsy. On gross examination, a berry aneurysm of the right middle cerebral artery causing marked compression of the right optic tract was found. Arteriosclerotic changes were observed microscopically in the right middle cerebral and in the internal carotid arteries. The left iris was markedly degenerated, with atrophy of the constrictor muscle. Compression of the right optic tract may cause homonimus hemianopsia. A dilated and unresponsive left pupil indicated a lesion in the ipsilateral parasympathetic efferent pathway. In the absence of appreciable lesions of the left oculomotor nerve, the most likely cause of mydriasis was the iridic lesion. Intracranial aneurysms are common in humans (2 to 5%), but not in other species. Only about 10% of unruptured aneurysms are associated with neurologic deficits related to mechanical compression, such as visual deficits or anisocoria. Meticulous investigation of the ocular vascular and neural pathways led us to conclude that the anisocoria was unrelated to the aneurysm. To our knowledge, this report represents the first documented case of a naturally occurring intracranial aneurysm in nonhuman primates.

Horner syndrome with equal-sized pupils in a case with underlying physiologic anisocoria.

A case is presented in which Horner syndrome occurred on the side of the larger pupil in underlying physiologic anisocoria. The unusual coincidence resulted in ipsilateral ptosis, but with clinically equal-sized and normally reactive pupils.