Visual Seizures Research Articles

Electroclinical characteristics of new-onset seizures associated with neurocysticercosis.

Although seizures are the most common presentation of neurocysticercosis (NCC), the electroclinical characteristics of the seizures have not been adequately studied. The study cohort included 308 consecutive patients presenting with a new-onset seizure, both acute symptomatic or unprovoked. They were divided into two groups: Group 1 (NCC group), those in whom imaging studies revealed active or inactive NCC (N = 184 (59.7%)) and group 2 (non-NCC group), those in whom either imaging was normal or revealed abnormalities other than NCC or the diagnosis was idiopathic generalized epilepsy (N = 124 (40.3%)). Clinical features significantly associated with group 1 included focal seizures (specifically, aphasic seizures (P < 0.05)), seizure clusters (P < 0.0001), postictal Todd's paresis (P < 0.05), and peri-ictal headaches (P < 0.008). In addition, somatosensory and visual seizures, and focal-clonic and focal-tonic were more frequent in this group. Generalized clonic seizures (P < 0.05) were significantly more common in the group 2. The findings of regional epileptiform abnormalities (P = 0.0001) and primary generalized epilepsy (P < 0.0001) on electroencephalography were significantly more common in group 2. In patients presenting with new-onset seizure, aphasic seizures, seizure clusters, postictal Todd's palsy and peri-ictal headaches might augur the finding of NCC, both active and inactive lesions, on imaging.

Case 2: A teenager with nausea, vomiting and dysarthria

A 13-year-old boy presented with a five-month history of nausea and morning vomiting not associated with headaches or abdominal pains. His bowel movements were normal. He had demonstrated weight loss and reported fatigue, drooling, choking and bilateral calf muscle cramps. There were no visual changes, ataxia, vertigo, rigidity, seizures or psychiatric disturbances. His neurological examination was significant for tongue fasiculations, dysarthria, and mild weakness and tremor in the right hand, with poor coordination. The remainder of his neurological examination was normal, with no papilloedema. The differential diagnosis included central nervous system neoplasia, a demyelinating disease, a neurodegenerative disease, a metabolic disorder and a bradykinetic movement disorder such as juvenile Parkinsonism. Other considerations included drug effects or toxicity, and endocrine disorders such as hyperthyroidism. An urgent brain magnetic resonance imaging was scheduled. His thyroid profile, drug screen, electrolyte levels and renal function were all normal. Magnetic resonance imaging demonstrated bilateral symmetrical striatal and tegmental lesions suggestive of necrosis and/or calcifications (Figure 1). There was diffuse brain atrophy with prominent ventricles, wide occipital horns and prominent pericerebral spaces. Figure 1) Axial fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging through the basal ganglia. Markedly increased FLAIR signal in the lentiform nuclei and caudate heads bilaterally, as well as the superimposed low signal, likely indicate mineralization ...

1205

Introduction: The posterior reversible encephalopathy syndrome (PRES) is manifested by headache and altered mental status with or without visual disturbances and seizures along with unique radiological findings. We present a case of 53 year old female with renal cell cancer who developed PRES after radical nephrectomy. Although PRES has been associated with hypertension and renal disease, and while there have been few case reports of postoperative PRES, this is the first case report to our knowledge of the syndrome occurring after a nephrectomy. A 53 year old female with well controlled hypertension and diabetes mellitus initially presented with several month history of weight loss, recurrent low grade fevers, and intermittent right lower quadrant pain. Upon imaging, she was found to have right renal mass with invasion of right renal vein and possible vertebral metastases. She underwent right radical nephrectomy with regional lymph node removal. On third post operative day, the patient developed chest pain and EKG changes and was started on anticoagulation with heparin along with aspirin and plavix. Subsequently on post operative day five, she started complaining of headache, nausea, vomiting and rapidly developed altered mental status and loss of vision without any other focal neurological weakness or ataxia. Previously well controlled blood pressure started to rise, with mean arterial pressure now ranging between 100-120 mm of Hg. Brain MRI revealed new onset edema tracking along the bilateral posterior occipital lobe white matter compatible with PRES. Also seen were right subarachnoid hemorrhage and intra-parechymal petechial hemorrhage. She received fresh frozen plasma and platelet transfusions along with strict blood pressure control with intravenous anti hypertensives. Patient had rapid recovery with resolution of altered sensorium over the next 24 hours and improvement in her visual symptoms in 48-72 hours. Patient was subsequently discharged home. We report a unique case of development of PRES syndrome occurring after nephrectomy. Our case highlights importance of early recognition of the syndrome and strict blood pressure control in such settings.

Severe Methanol Intoxication due to Spirit Consumption and Magnetic Resonance Imaging Findings

ABSTRACTOZET Introduction Methanol has a molecular weight of 32 g/mol. It is freely miscible with water, ethanol, and many organic solvents. Methanol is water-soluble and easily crosses the blood-brain barrier (1).Methanol poisoning has a rare incidence, however, it presents with a high morbidity and mortality. Generally, it is encountered after an attempted suicide or an accidental intake. Methanol poisoning affects the optic nerve and central nervous system, particularly the basal ganglia, potentially leading to visual impairment, blindness, diz-ziness, seizures, and coma (2, 3). Patients present with symptoms such as blindness, motor dysfunction, rigidity, hypokinesia, and other Parkinson-like signs (2, 4). In this study, we aimed to underscore the importance of MRI findings in a patient that presented with late signs of serious intoxication in whom we were unable to evaluate serum methanol and ethanol levels. Case Report A 32-year-old unconscious man was admitted to the Emergency Department because of vomiting and severe meta-bolic acidosis with an arterial pH of 6.79 (normal range 7.35-7.45). The anion gap was 32 mmol/L (8-16 mmol/L), whereas HCO

Bevacizumab for radiation necrosis following treatment of high grade glioma: a systematic review of the literature

This review identifies the current literature on the use of bevacizumab for cerebral radiation necrosis in patients with high-grade gliomas, summarizes the clinical course and complications following bevacizumab, and discusses the relative costs and benefits of this therapeutic option. A Medline search was conducted of all clinical studies before September 2012 investigating outcomes following use of bevacizumab therapy for radiation necrosis in patients with high-grade gliomas. Clinical and radiographic outcomes are reviewed. Seven studies reported a total of 30 patients with high-grade gliomas treated with bevacizumab for radiation necrosis. All patients demonstrated decreased radiographic volume of edema on T1 and T2 MRI sequences. Clinical outcomes were reported for 23 patients: 16 (70 %) had improvement in neurologic signs or symptoms, 5 (22 %) had mixed results, and 2 (9 %) remained neurologically unchanged. Complications were documented in 5 of 7 studies (18 of 29 patients, 62 %) and included deep vein thrombosis, pulmonary embolism, visual field worsening, worsening hemiplegia, pneumonia, seizure, and fatigue. Only one study evaluated quality of life measures and none evaluated cost or cost effectiveness. Data regarding the use of bevacizumab to treat radiation necrosis in patients with high-grade gliomas is limited and primarily class III evidence. While bevacizumab improves neurological symptoms and reduces radiographic volume of necrosis-associated cerebral edema, it comes at the expense of a high rate of potentially serious complications. Definitive evidence for the utility, cost-effectiveness, and overall efficacy of this management strategy is currently lacking and additional investigation is warranted.

Temporal Lobe Arteriovenous Malformations

Temporal lobe arteriovenous malformations (AVMs) represent a subgroup of intracranial AVMs with particular characteristics and management issues. To characterize the surgical outcomes of temporal lobe AVMs with emphasis on visual field deficits (VFDs) and seizures. Between 1992 and 2008, 29 patients were operated on for temporal lobe AVMs. Patient data were retrospectively collected and analyzed. Twelve of 29 patients (41.4%) presented with seizures and 4 (13.7%) presented with VFDs. Postoperatively, 6 patients (24%) showed new VFDs and 2 improved, with a rate of preservation of full visual fields of 84%. Larger AVMs (> 3 cm) were significantly associated with postoperative VFD (P = .008). Epilepsy outcomes assessed by the Engel scale were as follows: 9 patients (75%) were in class I (seizure free), 1 patient (8.3%) was in class III, and 2 patients (16.6%) were in class IV (no change or worsening). Postoperative modified Rankin Scale outcomes were excellent (grade 0-1) in 18 patients, good (grade 2) in 7, and poor (grade 3-4) in 4. Older age at diagnosis correlated with a worse functional outcome (Spearman ρ = 0.369; P = .049). AVMs were totally removed in 27 of 29 patients (93.1%). Complete surgical excision was confirmed with angiography. Two patients needed reoperation for AVM remnant. Three patients had persistent hemiparesis (10.3% permanent morbidity). There was no mortality. Seizure control is usually underappreciated in the surgical management of AVMs. However, in temporal lobe AVMs, good outcomes with low morbidity and good visual field preservation can be accomplished.

A 50‐Year‐Old Man with Back Pain and A Sellar Mass

Hepatocellular carcinoma rarely metastasizes to the pituitary gland and this site is very rarely the initial site of disease presentation. When it does, it may mimic a far more common pituitary adenoma. Metastatic hepatocellular carcinoma should be suspected in any individual with known liver disease or significant risk factors. The most common clinical sign of metastatic HCC to the skull is a subcutaneous mass followed by neurological deficits including visual disturbances, headache and seizure. The diagnosis can be made based on the histopathologic and immunohistochemical findings. When metastatic HCC is present in the skull base, appropriate work up should be done to rule out other metastatic sites, most commonly present in the spine.

Genetics of epilepsy syndromes in families with photosensitivity

To use family studies to investigate the clinical genetics of photosensitivity to understand the interrelationship of different photosensitive epilepsy syndromes. Twenty-nine families were recruited in which at least 2 members had idiopathic epilepsy and either clinical or electrical photosensitivity on EEG studies. We performed electroclinical analysis of these individuals and all other affected family members and analyzed the phenotypic patterns in families. An earlier age at seizure onset was observed in photosensitive patients compared with nonphotosensitive individuals. A significant female bias for photosensitivity was confirmed. All subjects with visual seizures were photosensitive. Subjects could be classified into 3 main photosensitive phenotypes: genetic (idiopathic) generalized epilepsies (GGE), idiopathic photosensitive occipital epilepsy (IPOE), and mixed GGE/IPOE. Within each category, subjects with purely photosensitive seizures were observed. We report a distinctive syndrome of early-onset photosensitive absence epilepsy, with onset beginning by 4 years of age, which was more refractory than childhood absence epilepsy. The clinical genetics of the idiopathic photosensitive epilepsies show a phenotypic spectrum from the GGEs to IPOE with overlap between the focal features of IPOE and all the GGE syndromes. Shared genetic determinants are likely to contribute to the complex inheritance pattern of photosensitivity, IPOE, and the GGEs.

Is it migralepsy? No evidence yet

There is a wide consensus about the need of an urgent revision of the current ICHD-II and ILAE criteria to properly represent the migraine/seizure relationships and to avoid confusion among neurologists subspecialized in headache or epilepsy treatment [1, 2]. In fact, the habit of epileptologists is to define an electroclinical event by EEG recordings while a classificative approach is commonly used by neurologists specialized in headache. The scepticism surrounding the concept of migralepsy, as a migraineepilepsy sequence, deriving by the findings of a recent work by Sances and colleagues [3]. Interestingly, the authors underscored the high prevalence of purely epileptic disorders among cases reported as migralepsy and, in particular, among the 50 potential migralepsy cases identified in the literature only two meet the current ICHD-II criteria supporting a diagnosis of migralepsy [3]. Colombo et al. [1] recently described the case of a usual episode of visual aura, lasting 15 min, followed by the appearance of clonic palpebral movements and a generalized seizure in a 43-year-old woman patient who suffered of migraine with aura. The authors conclude that the sequence of the clinical picture supports the diagnosis of migralepsy in this case, accordingly to the current ICHD-II criteria [1]. Unfortunately, Colombo et al. failed to provide any ictal EEG recording of the sequence visual aura-generalized seizure. In this sense, the ictal recordings of the sequence are necessary to achieve firm conclusions about the epileptic nature of the visual aura that appear before a generalized seizure. Interestingly, their patient showed clonic palpebral movements before the generalized seizure onset. Noteworthy, patients with idiopathic generalized epilepsy experience visual aura and this visual phenomenon is more frequent in eyelid myoclonia patients with absences syndrome [4]. Thus, in our opinion, the concept of migralepsy should be revised keeping in the mind that visual symptoms can be the epileptic ‘‘aura’’ of a seizure, as it has been shown in the case description of patients with a partial status epilepticus in occipital lobe epilepsy [2] or migralepsy [3]. Of note, the EEG recording reported after the generalized seizure showed a focal epileptic discharge during the complaining of a severe migraine attack by the patient [1]. This finding reinforces the new introduced concept of ictal epileptic headache (IEH) [5, 6]. In fact, over the last 10 years, several cases of headache/migraine as sole manifestation of an epileptic seizure have been well documented by EEG recordings and the term IEH have been proposed to define an epileptic seizure with migraine/ headache like features [6, 7]. Unlike IEH, the clinical picture of migralepsy according to the ICHD-II criteria represents a very rare and no recurrent phenomenon in clinical practice. This feature should be kept in the mind because migraine and epilepsy are the prototypes of chronic diseases with paroxysmal episodes. On the other hand, there seems to be more V. Belcastro (&) Neurology Clinic, S. Anna Hospital, 22020 Como, Italy e-mail: vincenzobelcastro@libero.it

Siblings with refractory occipital epilepsy showing localized network activity on EEG‐fMRI

The benign occipital epilepsies of childhood include Panayiotopoulos and Gastaut syndromes; a third syndrome, idiopathic photosensitive occipital epilepsy may also begin in childhood or adolescence. We describe siblings with occipital epilepsy characterized by refractory, frequent, brief visual seizures and normal magnetic resonance imaging (MRI). Electroencephalography (EEG) with functional MRI (fMRI) supports localization of interictal epileptiform activity to the occipital lobes. Our hypothesis is that the siblings share a genetic focal epilepsy arising from a localized occipital network. Although they share many features of Gastaut syndrome, their refractory ongoing seizures in adolescence is unusual and likely due to underlying genetic determinants.

Predicting levels of independence with expressing needs and ideas 1 year after severe brain injury.

Severe brain injury (BI) is a catastrophic event often evolving into a complex chronic and severely disabling condition making activity participation possible only with sustained caregiving. One aspect of building sustainable caregiving is early provision of information about expected outcomes germane to patients and their caregivers. An analysis was conducted to determine whether 2 levels of independence with expressing needs and ideas 1-year after severe BI could be predicted using variables available early after injury. The authors examined a subsample (n = 79) of participants of an outcome study who received repeated neurobehavioral evaluations with the Disorders of Consciousness Scale (DOCS) and who were assessed 1 year after injury with the Functional Independence Measures (FIM). Explanatory variables included DOCS measures, patient characteristics, coexisting conditions, and interventions. The outcome is measured with the FIM Expression item. Optimal data analysis was used to construct multivariate classification tree models. The 2nd (p = .004) DOCS visual measure and seizure (p = .004) entered the final model providing 79% accuracy in classifying more or less independence with expressing needs and ideas at 1 year. The model will correctly identify 78% of future severe BI survivors who will have more independence and 82% of persons who will have less independence. For persons incurring severe BI, it is possible to predict, early after injury, more and less independence with expressing needs and ideas 1-year after injury. This evidence is 1 contribution to a larger body of evidence needed to enable early caregiver education about recovery expectations in terms of patient functioning relative to caregiving needs, which in turn will help build sustainable caregiving for this population.

Irreversible Hemorrhagic Complication of Recurrent Posterior Reversible Encephalopathy Syndrome in a Patient with Systemic Lupus Erythematosus

A diagnosis of posterior reversible encephalopathy syndrome (PRES) is based on a combination of clinical symptoms including headache, altered alertness, abnormalities of visual perception, and seizure, and characteristic neuroimaging findings of transient white matter edema, mostly in the posterior parietal-temporaloccipital regions of the brain (1, 2). Conditions commonly associated with PRES include severe hypertension, eclampsia/ preeclampsia, immunosuppressive medications including cyclosporine and taclorimus, antineoplastic agents, and various cause of renal failure (3, 4). PRES as a complication of systemic lupus erythematosus (PRES-SLE) is not uncommon and neurologic or psychiatric abnormalities occur in up to two-thirds of patients with SLE (4). Usually PRES is reversible vasogenic edema in the posterior circuation territories, although atypical findings such as conversion to irreversible cytotoxic edema, hemorrhage, and enhancement have been described (3). And cytotoxic edema surrounded by extensive vasogenic edema resulted in poor outcome. We report a case of PRESSLE showing irreversible hemorrhagic transformation as a complication of recurrent PRES.

Effect of Hydroxychloroquine on Visual System in Patients with Systemic Lupus Erythematosus using Visual Evoked Potential

Aim: This study was performed to determine the effect of Hydroxychloroquine on visual system in patients with systemic lupus erythematosus.Materials and methods: In a cross -sectional study, 50 subjects (without visual problem and seizure) including 25 with and 25 without systemic lupus erythematosus under treatment with chloroquine were selected. Visual evoked potential test was performed in two groups.Results: The mean amplitude was 6.04 in case and 5.84 μ∉- ι∈1/2 χo∈1/2∉ρoΔ γρo∉..π ωηιχη σηoωσ ∈1/2o σ∉α∉ισ∉ιχαΔΔψ σιγ∈1/2ιϕιχα∈1/2∉ διϕϕeρe∈1/2χe.The mean latency was 100.50 in case and 95.35 msec in control group which is not statistically significant.Conclusion: Based on the result of present work one can conclude that hydroxychloroquine has no adverse effect on visual pathway which will be discussed in detail in full paper.

Septo-optic dysplasia complex: Clinical and radiological manifestations in Omani children

Background:Septo-optic dysplasia (SOD), also known as de-Morsier's syndrome, is a rare disorder characterized by any combination of optic nerve hypoplasia (ONH), pituitary gland hypoplasia, and midline abnormalities of the brain including absence of septum pellucidum and corpus callosum dysgenesis. It is typically diagnosed in infancy and has a variable presentation that includes visual, neurologic, and/or hypothalamic-pituitary endocrine deficits.Purpose:To demonstrate the ophthalmic, endocrine, and neurologic spectrum of SOD in five Omani children and address the crucial role of high-resolution neuroimaging for its early and accurate diagnosis.Materials and Methods:A retrospective chart review was performed in 2010 of all children in the pediatric ophthalmology database of Sultan Qaboos University Hospital (SQUH) who were diagnosed to have ONH. All relevantdemographic, ophthalmic, neurologic, endocrine, and neuro-radiological manifestations were recorded in a data collection form. All previous neuroimaging results were reviewed by a neuro-radiologist.Results:Five patients (four males, one female) with the diagnosis of ONH were included in the study. They presented during the period 1998-2008. All patients were born at term, with normal birth weights to healthy mothers with insignificant antenatal history. Age at presentation ranged from three months to one year. Manifestations at presentation included severe visual impairment (5/5), neonatal hypoglycemia (3/5), seizure disorder (2/5), and failure to thrive (4/5). ONH was bilateral in 3/5 patients and unilateral in (2/5). Brain and orbit imaging revealed varying anomalies in all patients. These included absent septum pellucidum (3/5), severe corpus callosum agenesis (1/5), ectopic pituitary (5/5), falx cerebri deficiency (1/5), optic nerve hypoplasia (5/5), optic chiasmal hypoplasia (5/5), and olfactory tract hypoplasia (1/5). Endocrine deficits were detected in 4/5 patients (3 with panhypopituitarism, and 1 with growth hormone deficiency) and necessitated replacement therapy.Conclusion:SOD is a clinically heterogeneous disorder with a wide spectrum of ophthalmic, endocrine, and neurologic manifestations. All features might not be present in a single patient. A high consanguinity rate and lack of history of alcohol and drug use were observed in our cohort. Most affected children present first to the pediatrician with failure to thrive. Radiological confirmation of ONH necessitates high-resolution imaging and interpretation by an experienced neuro-radiologist. In our cohort, all patients with ONH had associated optic chiasmal hypoplasia. Early detection and treatment reduces disease-related morbidity, and can be life saving.

Visual Seizure: A Reversible Complication of Non-Ketotic Hyperglycemia

A 65-year-old man with diabetes mellitus was presented with left visual aura, followed by a versive seizure, each lasting approximately 3 minutes. Neurological examination showed an intermittent left homonymous hemianopsia. Brain magnetic resonance imaging (MRI) showed right occipital lobe lesion, with cytotoxic edema. Blood glucose was 593 mg/dL and serum osmolarity was 309 mOsm/kg. The seizures were controlled by normalization of blood sugar and short-term anticonvulsant, and the lesions were resolved in a follow-up MRI. We report a case of visual seizures associated with non-ketotic hyperglycemia. (Endocrinol Metab 27:155-158, 2012)

From migraine to epilepsy: a threshold mechanism?

A 67-year-old man complained of a transient blurring of vision in his right visual field lasting 30 min followed by headache. Two weeks later, the visual disturbance changed its pattern; it was described as the occurrence of brown round-shaped images in the right visual field spinning and turning for few seconds. This evolution from visual aura to visual seizures, with video-EEG correlation, supports the hypothesis of modification in threshold of cortical hyperexcitability from migraine to epilepsy.

Neurodegeneration and functional impairments associated with glycogen synthase accumulation in a mouse model of Lafora disease

Lafora disease (LD) is caused by mutations in either the laforin or malin gene. The hallmark of the disease is the accumulation of polyglucosan inclusions called Lafora Bodies (LBs). Malin knockout (KO) mice present polyglucosan accumulations in several brain areas, as do patients of LD. These structures are abundant in the cerebellum and hippocampus. Here, we report a large increase in glycogen synthase (GS) in these mice, in which the enzyme accumulates in LBs. Our study focused on the hippocampus where, under physiological conditions, astrocytes and parvalbumin-positive (PV+) interneurons expressed GS and malin. Although LBs have been described only in neurons, we found this polyglucosan accumulation in the astrocytes of the KO mice. They also had LBs in the soma and some processes of PV+ interneurons. This phenomenon was accompanied by the progressive loss of these neuronal cells and, importantly, neurophysiological alterations potentially related to impairment of hippocampal function. Our results emphasize the relevance of the laforin–malin complex in the control of glycogen metabolism and highlight altered glycogen accumulation as a key contributor to neurodegeneration in LD.

Recurrent occipital seizures misdiagnosed as status migrainosus

Periictal headache is commonly reported in patients with epilepsy and often exhibits migraine features. Misdiagnosis is frequent since visual seizures may often be misinterpreted as visual aura of migraine. We herein describe a 35-year-old woman with recurrent occipital seizures, clinically presenting with intractable headache. EEG monitoring was crucial in order to reach the correct diagnosis.

Migraine triggered seizures and epilepsy triggered headache and migraine attacks: a need for re-assessment

In this issue of the Journal, Belcastro and associates review terminology and classification issues for migralepsy, hemicrania epileptica, post-ictal and ictal headache [1]. They raise key points such as ictal headache and visual seizures are often misdiagnosed as migraine, “migralepsy” is unlikely to exist and an “epilepsy-migraine sequence” is much more common and well documented than the dominant view of a “migraine-epilepsy sequence”. Their relevant proposals need appropriate attention by the committee of the international classification of headache disorders (ICHD) as well as the physicians in their clinical practice because of the consequences that misdiagnosis may have on patients. Misdiagnosis between epilepsy and migraine is considerable though their differentiation should not be difficult on clinical grounds [2]. The problem is that emphasis is unduly placed on individual symptoms, rather than on a comprehensive synthetic analysis of their quality, chronological sequence and other clustering features. There are many examples of such errors where visual seizures are unquestionably diagnosed as acephalgic migraine and more often migraine with aura (if seizures are followed by post-ictal headache) or basilar migraine with occipital paroxysms (which does not exist, because this is a syndrome of idiopathic childhood occipital epilepsy). Elementary visual hallucinations of occipital seizures develop rapidly within seconds, are brief in duration (2–3 min), are usually coloured and circular. These are fundamentally different from the visual aura of migraine, which develops slowly in minutes, is longer lasting (≥5 min) and mainly achromatic with linear patterns [3].

Disseminated nocardiosis masking an atypical zygomycosis presentation in a kidney transplant recipient

Immunosuppressive agents increase the vulnerability of solid organ transplant patients to opportunistic infections. An atypical clinical presentation of a bacterial and fungal co-infection makes diagnosis and treatment even more challenging in this population. A 54-year-old hypertensive woman underwent a cadaveric kidney transplant after years on hemodialysis. Her treatment included mycophenolate, tacrolimus, and prednisone. By post-transplant week 8, she had pneumonia followed by progressive visual changes and seizures. Diagnostic work-up, consisting of magnetic resonance imaging of the brain and chest x-ray, showed several cerebral ring-enhancing lesions, and a pulmonary cavitary lesion. Disseminated nocardiosis was suspected and therapy was started. Skin biopsy was taken from a nodular lesion and culture confirmed Nocardia species infection. During hospitalization, neurological deficit persisted with worsening of brain lesions. She underwent excision of a brain abscess and the final pathologic report showed mucormycosis, revealing the patient's co-infection by 2 different pathogens. After therapy with liposomal amphotericin B and posaconazole, she has remained stable for more than 1 year. Disseminated nocardiosis masked and delayed the diagnosis and treatment of a more aggressive and worrisome organism. Mucormycosis, as a non-fatal isolated brain abscess without rhinal involvement, is an atypical presentation, and only a few cases have been reported.