Autoimmune Cerebellar Ataxia: Etiology and Clinical Characteristics of a Case Series from China.

Autoimmune cerebellar ataxia (ACA) is an important and potentially treatable cause of sporadic cerebellar syndrome, but studies with large sample size are limited. This study reported a large ACA series in China and described its etiology and clinical characteristics. We reviewed all ACA patients from our hospital (2013-2021) and analyzed their clinical and paraclinical features, treatment, and outcome. ACA subtypes investigated included paraneoplastic cerebellar degeneration (PCD), primary autoimmune cerebellar ataxia (PACA), anti-glutamate decarboxylase (GAD)-associated cerebellar ataxia, opsoclonus-myoclonus syndrome (OMS), Miller Fisher syndrome (MFS), and ACA-associated with autoimmune encephalitis. A total of 127 patients were identified and 40.9% were male. The median onset age was 47.0 years. Gait ataxia was the most prevalent feature followed by limb ataxia, dizziness, and dysarthria/dysphagia. Extracerebellar manifestations included pyramidal signs (28.3%) and peripheral neuropathy/radiculopathy (15.0%). ACA subtypes were PCD (30.7%), PACA (37.8%), ACA associated with autoimmune encephalitis (12.6%), anti-GAD-associated ACA (8.7%), MFS (7.1%), and OMS (3.1%). Neuronal antibodies were positive in 67.7% of patients. Brain magnetic resonance imaging was unremarkable (55.7%) or showed atrophy (18.3%) or abnormal signal intensity (26.1%, most of which was extracerebellar). Although most patients received immunotherapy, the modified Rankin scale at last follow-up was ≤ 2 in only 47.3% patients. Thirteen patients died and 24 relapsed. Compared with PACA, PCD patients were older and had poorer outcome. This study illustrates the heterogeneity in the clinical features of ACA and suggests the importance of neuronal antibody testing in ACA diagnosis. PCD and PACA are the dominant ACA subtypes, and the former has a less favorable prognosis.

A Systematic Review on Anti-Yo/PCA-1 Antibody: Beyond Cerebellar Ataxia in Middle-Aged Women with Gynecologic Cancer.

Current understanding of anti-Yo/PCA1 antibody-associated cerebellar ataxia is based on case reports and small case series. Our goal was to summarize clinical features, highlighting atypical presentations and gaps of knowledge. Following the PRISMA guidelines, we systematically screened Pubmed/MEDLINE, Embase, Scopus, and Web of Science from inception to April 2022 for all case reports and series concerning anti-Yo antibody-associated cerebellar ataxia. We collected data on clinical presentation, investigation findings, and treatment outcomes. Of 379 included patients, 96% were female with gynecologic cancer (82%). Among men, 87% had an associated tumor, mainly of gastrointestinal origin. The median age was 60 years old. Pancerebellar ataxia was the main clinical feature, but extracerebellar findings were frequent during the disease course. Vertigo and imbalance can be present early in the disease course in about two thirds of patients, as a prodromal phase. Although neuroimaging usually is normal or shows cerebellar atrophy, inflammatory changes may also be present. More than half of the patients reported some improvement after immunotherapy. However, despite treatment, 84% of survivors were unable to walk unassisted on follow-up. Our study provides objective data and advances in current knowledge of anti-Yo antibody-associated cerebellar ataxia such as the description of prodromal symptoms, extracerebellar findings, and its presentations in males.

Paraneoplastic Cerebellar Degeneration (PCD) associated with PCA-1 antibodies in established cancer patients.

INTRODUCTION: Paraneoplastic cerebellar degeneration (PCD) is a rare set of neurological disorders arising from tumor-associated autoimmunity against antigens within the cerebellum. Anti-Purkinje cell cytoplasmic antibody 1 (PCA-1), or anti-Yo, is the most commonly linked antibody and is classically associated with breast and ovarian cancers. METHODS: Medical records of patients at our institution who developed PCA-1 associated PCD were reviewed. Clinical information, including cancer history, cancer-directed treatment, and serum and CSF titers of PCA-1 antibody were extracted. CASES: We report a series of cases of PCA-1 associated PCD in patients with known breast or ovarian cancer diagnosis not receiving immunotherapy. These cases highlight aspects of PCA-1 paraneoplastic syndrome such as triggering by cytotoxic chemotherapy or surgery, the possibility of tumor recurrence and the association with development of a second cancer. DISCUSSION: Diagnosis of the syndrome requires neurological workup with lumbar puncture (LP) with cerebrospinal fluids (CSF) studies, serum and CSF paraneoplastic antibody panel, and neuroimaging. Inpatient admission for prompt workup and initiation of treatment is recommended. Treatment most commonly includes immunosuppression with corticosteroids, plasmapheresis, and/or intravenous immune globulin (IVIG); however, we postulate that other immune modulating treatments may warrant consideration. CONCLUSION: These cases highlight the need for early recognition of the syndrome in patients receiving nonimmune based chemotherapy, for prompt workup and treatment.

Plasma exchange for treating anti-Yo-associated paraneoplastic cerebellar degeneration: Case report and literature review.

RATIONALE: Paraneoplastic cerebellar degeneration (PCD) is a rare neurodegenerative syndrome associated with antibodies targeting the Purkinje cells of the cerebellum. Most cases of anti-Yo-associated PCD occur in females, with <20 cases reported in males. Herein, we report a male patient with anti-Yo-associated PCD who was treated with plasma exchange and achieved a favorable outcome. PATIENT CONCERNS: A 64-year-old man presented with progressive ataxia, gait instability, and dysuria. Electroencephalography, electromyography, brain and spinal neuroimaging, and routine laboratory examinations were all normal. The anti-neuronal antibody Anti-Yo was detected in the serum but not in the cerebrospinal fluid (CSF). DIAGNOSIS: The patient was diagnosed with definite anti-Yo-associated PCD based on the clinical manifestations, anti-Yo was detected in the serum and response to treatment. INTERVENTIONS: At beginning, the patient was treated with dexamethasone (10 mg/day for 10 days). Then, plasma exchange was performed. OUTCOMES: After treated with dexamethasone, no clinical improvement was noted in this patient. In the following month, his condition deteriorated. However, after two courses of plasma exchange, neurological examination showed marked improvement in gait. After four courses of plasma exchange, the patient could walk independently, the Romberg test was negative, and anti-Yo antibodies were undetectable. At the 6-month follow-up, the patients' symptoms were relieved, and tests for anti-Yo antibodies remained negative. LESSONS SUBSECTIONS: Treatment with plasma exchange for anti-Yo-associated male PCD patients without a concomitant tumor are recommend and need more studies.

Paraneoplastic Cerebellar Degeneration in Nasopharyngeal Carcinoma: a Unique Association.

Paraneoplastic cerebellar degeneration (PCD) is a rare disorder that is associated with lung or gynecological malignancies and Hodgkin lymphoma. Neurologic symptoms are commonly the initial presenting sign leading to the diagnosis of an underlying malignancy. We are presenting an Asian male with progressive lower extremity weakness with EBV-positive nasopharyngeal carcinoma (NPC) and anti-Yo antibodies. Peculiarly, transient diffuse leptomeningeal enhancement is seen on MR imaging. This is the first report of PCD associated with NPC and thus illustrates that PCD embodies a boarder set of disease than previously described.

[Paraneoplastic Cerebellar Degeneration with Lambert-Eaton Myasthenic Syndrome: A Report of an Effectively Treated Case and Systematic Review of Japanese Cases].

A 63-year-old female who developed dizziness, diplopia and subsequent gait disturbance from September X-1 year was analyzed. The first neurological findings in May X year revealed cerebellar ataxia, weakness in the proximal limbs, decreased tendon reflexes, and autonomic symptoms (ADL:mRS 3). Furthermore, an incremental phenomenon was observed in the repetitive nerve stimulation test, and she was diagnosed with Lambert-Eaton myasthenic syndrome (LEMS) based on the serum P/Q-type calcium channel (VGCC) antibody positivity. In addition, small cell lung cancer was detected by chest CT and bronchoscopy, and her cerebellar ataxia was diagnosed as paraneoplastic cerebellar degeneration (PCD). Therefore, the patient underwent chemotherapy and radiotherapy from June in X year. Six months after initiation of treatment, her cerebellar ataxia had almost disappeared and she could walk without assistance (ADL:mRS 1). The P/Q-type VGCC antibodies were also negative at that time. Cases wherein cerebellar ataxia resolved almost completely in parallel with disappearance of the serum P/Q-type VGCC antibodies are of great interest. We conducted a systematic literature review of PCD-LEMS cases in Japan reported since P/Q-type calcium channel antibody measurement was reported in 1995. As a result, 13 cases (including our study) that concurrently displayed cerebellar ataxia and LEMS were selected. The average age of the 13 patients (10 males and 3 females) was 61.5 years. Small cell carcinoma was complicated in 11 patients (10 in the lung and 1 in the oropharynx); in the other 2 patients, cancer was not found at the time of reporting (the observation period was as short as 1-2 months). The time from onset to treatment ranged between 1 week and 10 months. While 1 of the 13 patients developed cerebellar ataxia during the subsequent course of the treatment, the remaining 12 had already developed cerebellar ataxia and LEMS symptoms, although their main neurologic finding was cerebellar ataxia and they were subsequently diagnosed with LEMS after electrophysiological testing and autoantibody detection. Small cell carcinoma was found in 11 patients. We define the pathology following such a certain clinical course as PCD-LEMS. The P/Q-type VGCC antibodies were positive in 11 of the 13 cases, although their antibody titers were not necessarily very high. Treatment for the associated small cell carcinoma might have improved the neurological findings in 9 of the 11 PCD-LEMS patients. The P/Q-type VGCC antibodies were measured before and after the treatment. The PCD-LEMS symptoms improved in all patients and their antibody titers decreased. These findings indicate that P/Q-type VGCC antibodies are involved in the pathology of PCD-LEMS. Appropriate and timely treatment, at least in PCD-LEMS patients in Japan, that actively treats any associated cancer can be expected to improve not only life prognosis but also cerebellar ataxia. (Received October 15, 2018; Accepted November 5, 2018; Published January 1, 2019).

TRIM9 and TRIM67 Are New Targets in Paraneoplastic Cerebellar Degeneration.

To describe autoantibodies (Abs) against tripartite motif-containing (TRIM) protein 9 and 67 in two patients with paraneoplastic cerebellar degeneration (PCD) associated with lung adenocarcinoma. Abs were characterized using immunohistochemistry, Western blotting, cultures of murine cortical, and hippocampal neurons, immunoprecipitation, mass spectrometry, knockout mice for Trim9 and 67, and cell-based assay. Control samples included sera from 63 patients with small cell lung cancer without any paraneoplastic neurological syndrome, 36 patients with lung adenocarcinoma and PNS, CSF from 100 patients with autoimmune encephalitis, and CSF from 165 patients with neurodegenerative diseases. We found Abs targeting TRIM9 and TRIM67 at high concentration in the serum and the cerebrospinal fluid (CSF) of a 78-year-old woman and a 65-year-old man. Both developed subacute severe cerebellar ataxia. Brain magnetic resonance imaging found no abnormality and no cerebellar atrophy. Both had CSF inflammation with mild pleiocytosis and a few oligoclonal bands. We identified a pulmonary adenocarcinoma, confirming the paraneoplastic neurological syndrome in both patients. They received immunomodulatory and cancer treatments without improvement of cerebellar ataxia, even though both were in remission of their cancer (for more than 10 years in one patient). Anti-TRIM9 and anti-TRIM67 Abs were specific to these two patients. All control serum and CSF samples tested were negative for anti-TRIM9 and 67. Anti-TRIM9 and anti-TRIM67 Abs appeared to be specific biomarkers of PCD and should be added to the panel of antigens tested when this is suspected.

Paraneoplastic cerebellar degeneration as a manifestation of metastatic recurrent carcinoma breast: rare scenario.

Carcinoma breast presenting with paraneoplastic cerebellar degeneration is a rare scenario. We report a case of a 52-year-old woman, which is a follow-up case of completely treated carcinoma breast presenting with paraneoplastic cerebellar degeneration which, on investigation, revealed metastatic disease with recurrence at previous scar site and metastasis to contralateral axilla. The patient was given pulse methyl prednisolone therapy and underwent wide local excision of nodule and right axillary lymph node dissection with 14 cycles of trastuzumab and paclitaxel as adjuvant therapy. However, there was no detectable change in neurological symptoms at 6-month follow-up postoperatively. This case report highlights the need for clinicians to be aware of all possible presentations of carcinoma breast and its recurrence, including rare manifestations as in this case.

Paraneoplastic cerebellar degeneration associated with cerebellar hypermetabolism: Case report.

RATIONALE: Paraneoplastic cerebellar degeneration (PCD) is an immune-mediated neurological deficit affecting the cerebellum. Anti-Yo antibody positive PCD is a rare occurrence most likely associated with gynecologic or breast malignancies. The identification of the underlying tumor is a diagnostic challenge in many of these patients. PATIENT CONCERNS: We present a 68-year-old woman with acute symptoms of PCD as a first sign of underlying occult malignancy. Further investigation revealed a positive anti-Yo antibody. Although brain magnetic resonance imaging (MRI) was unremarkable, positron emission tomography (PET)/computed tomography (CT) revealed intense hypermetabolism of cerebellum and diffused hypometabolism in the rest of brain. On 1-year follow-up, despite the primary malignancy is still unknown, her symptoms improved significantly after immunotherapy. DIAGNOSES: Paraneoplastic cerebellar degeneration. INTERVENTIONS: The patient was given IV methylprednisolone 500 mg once a day for 5 consecutive days, followed by oral prednisone 60 mg once a day for 3 months. OUTCOMES: The patient's symptoms were gradually improved during the hospitalization period. On one year follow up, she was able to walk independently and perform some simple tasks. LESSONS: Cerebellar hypermetabolism in PCD suspected patients may help confirming the diagnosis in an earlier stage and may predict a better outcome after immunotherapy.

Anti-Yo antibody-mediated paraneoplastic cerebellar degeneration associated with cognitive affective syndrome in a patient with breast cancer: a case report and literature review.

Breast cancer is the most common cancer in women, with 15%-25% of those tumours overexpressing the human epidermal growth factor receptor 2 (her2), which is associated with more aggressive disease. On rare occasions, patients present with a paraneoplastic syndrome months to years before their cancer diagnosis. Paraneoplastic cerebellar degeneration (pcd) is associated with fewer than 1% of cancers and is strongly associated with breast and gynecologic malignancies. Anti-Yo antibody is the antibody most frequently identified with the syndrome, and it is associated with a very poor prognosis. Recent studies have implicated a relationship between overexpression of her2 and anti-Yo-mediated pcd. Current pcd treatments include tumour removal, chemotherapy, targeted therapy, and immune-suppressive treatments. Outcomes of pcd are typically poor, and no guidelines for treatment currently exist. Early recognition followed by rapid initiation of treatment remains the cornerstone of therapy. Here, we present a case of anti-Yo-antibody pcd secondary to estrogen and progesterone receptor-negative, her2-positive breast cancer. Despite treatment with mastectomy, chemotherapy, and her2-targeted therapy, no significant neurologic improvement was achieved, and cerebellar cognitive affective syndrome subsequently developed.

A case of slowly progressive anti-Yo-associated paraneoplastic cerebellar degeneration successfully treated with antitumor and immunotherapy.

We report a case of slowly progressive anti-Yo-associated paraneoplastic cerebellar degeneration (PCD) with breast cancer in a 54-year-old woman. The symptoms of limb and truncal ataxia, and dysarthria gradually progressed during the course of 1 year, and the modified Rankin scale (mRS) score was 2. A mastectomy with sentinel lymph node resection was performed for the breast cancer. No malignant cells were found on histopathological examination of the lymph node. Combination chemotherapy with adriamycin and cyclophosphamide (AC) prevented neurologic deterioration. However, subsequent treatment with trastuzumab and paclitaxel did not prevent progression of the symptoms (mRS score 3). Brain magnetic resonance imaging showed atrophy of the cerebellar hemispheres without brain stem atrophy. Anti-Yo antibody was detected in the serum, which led to a diagnosis of anti-Yo-associated PCD. We resected an enlarged axillary lymph node, which was found on computed tomography. The histopathological analysis of the lymph node revealed foreign body granuloma, which suggested an association with necrotic malignant tissue. Following additional tegafur-uracil therapy and two courses of intravenous immunoglobulin (IVIg), the cerebellar signs and symptoms gradually improved (mRS score 2). The clinical course shows that PCD can present as a slowly progressive cerebellar symptom. We propose an active treatment for anti-Yo-associated PCD consisting of tumor resection, combined chemotherapy, and IVIg.

Voltage-Gated P/Q-Type Calcium Channel Antibodies Associated With Cerebellar Degeneration.

BACKGROUND: Paraneoplastic cerebellar degeneration is a rare neurological condition characterized by diffuse cerebellar dysfunction and magnetic resonance imaging evidence of progressive cerebellar atrophy. It has been associated with several autoantibodies and malignancies in adults. To date, only six cases have been described in male children. PATIENT DESCRIPTION: We describe an eight-year-old girl with a prodrome of abdominal pain and vomiting followed by acute onset diplopia, dysarthria, dysmetria, and ataxia. She was found to have cerebellar degeneration in association with P/Q-type calcium channel antibodies. CONCLUSION: This is the first child with documented paraneoplastic cerebellar degeneration in association with P/Q-type calcium channel antibodies.

Rapid Eye Movement Sleep Behavior Disorder in Paraneoplastic Cerebellar Degeneration: Improvement with Immunotherapy.

STUDY OBJECTIVES: To report two female patients with paraneoplastic cerebellar degeneration (PCD) related to breast cancer that presented with rapid eye movement-sleep behavior disorder (RBD) and improved sleep symptoms with immunotherapy. METHODS: The two patients were evaluated through clinical scale and polysomnography before and after therapy with intravenous immunoglobulin. RESULTS: RBD was successfully treated with immunotherapy in both patients. Score on the RBD screening questionnaire dropped from 10 to 1 or 0, allied with the normalization of polysomnographic findings. CONCLUSIONS: A marked improvement in RBD after immunotherapy in PCD raises the hypothesis that secondary RBD may be an immune-mediated sleep disorder.

Breast cancer revealed by a paraneoplastic cerebellar syndrome: about one case and literature review.

To describe a case of breast cancer manifested by cerebellar syndrome and to establish a relationship between breast cancer and Paraneoplastic syndromes through the presence of anti- yo antibodies in serum and cerebrospinal fluid of a patient. Our patient was 52 years old, Multipara with 5 children alive. She had been 3 years post-menopausal under Hormonal Replacement Therapy. Weight: 46.7 Kg; Height: 1.60 m; Body Surface Area: 1.59 m(2). Nil history of alcohol or tobacco smoking. Nil history suggestive of malignancies or autoimmune diseases. Her Blood group was oRh positive, nil presence of irregular agglutinins. She was admitted to the neurology service for vertigo and it was determined an isolated cerebellar syndrome. All tests were negative including tumor markers and radiological imaging. The clinical gynecological examination was perfectly normal. The diagnosis hypothesis was "meningo-encephalocerebellitis of viral origin" but with persistence and aggravation of the cerebellar syndrome, despite treatment. We decided to search, antibodies, anti-Hu, anti-Yo, anti-Ri, and anti Ta. Anti Yo was positive + + + in the cerebrospinal fluid and serum of the patient. The search for a gynecological cancer included a mammography which revealed micro calcifications in the left breast + + +. A lumpectomy of the left breast accompanied with x-ray identification of the micro calcifications was done and the histology showed a High Grade Intraductal carcinoma of the left breast with two homes of 3mm and 1 mm, corresponding to an infiltrating carcinoma of the left breast, grade II tumor of Scarff and Bloom (SBRII, 21 N + / 26, RH +, low Ki 67) and Estrogen and progesterone receptor positive +: multifocal cancer. Following the lumpectomy, mastectomy with ganglion clearing was done with adjuvant chemotherapy (FEC 6 Cycles): histology still showed Infiltrating Intraductal Carcinoma of the left breast, grade II tumor of Scarff and Bloom. Radiotherapy was followed and he patient was placed on hormonal therapy with Tamoxifen. The Patient's general condition was good with regression of cerebellar syndrome. Anti-Yo auto antibodies are quasi-specific for gynecological or breast tumors. Several hypotheses have been advanced on the pathophysiology and one wonders if someday, it will fail to do a very early diagnosis of cancer, including the breast cancers on the basis of the antigen-antibody reaction.

Responses to and Outcomes of Treatment of Autoimmune Cerebellar Ataxia in Adults.

IMPORTANCE: Classic Purkinje cell cytoplasmic antibody type 1 (PCA-1, or anti-Yo) paraneoplastic cerebellar ataxia has a poor prognosis, yet little has been published otherwise regarding treatment responses and outcomes among patients with autoimmune cerebellar ataxia. OBJECTIVES: To investigate treatment responses and outcomes in adults with autoimmune cerebellar ataxia. DESIGN, SETTING, AND PARTICIPANTS: A cohort study conducted at Mayo Clinic, Rochester, Minnesota, included 118 patients who had ataxia, were 18 years or older, were seropositive for at least 1 neural autoantibody, had received at least 1 immunotherapy or cancer therapy, and had neurologist-reported outcomes documented from January 1, 1989, through December 31, 2013. Data were collected from May 14, 2013, through August 9, 2014, and analyzed from August 9, 2014, through April 27, 2015. Responses to immunotherapy (corticosteroids, intravenous immunoglobulin, plasma exchange, and immunosuppressants) and ambulatory outcomes were compared between different subgroups. Subgroups were classified as paraneoplastic vs nonparaneoplastic disorders; neuronal nuclear and/or cytoplasmic (NNC) antibody positivity vs plasma membrane protein (PMP) antibody positivity; and glutamic acid decarboxylase 65-kDa isoform (GAD65) antibody positivity vs PMP antibody positivity. MAIN OUTCOMES AND MEASURES: Response to therapy and ambulatory ability, with univariate logistic regression and Kaplan-Meier analyses. RESULTS: Inclusion criteria were met by 118 patients. Median age at onset of neurologic symptoms was 58 (range, 27-83) years, and 87 patients (73.7%) were women. Median duration from symptom onset to last follow-up was 25 (range, 2-223) months. Sixty-three patients had paraneoplastic and 55 patients had nonparaneoplastic ataxic disorders. Eighty-one patients were seropositive for NNC antibodies (most commonly PCA-1 [anti-Yo], antineuronal nuclear antibody type 1 [anti-Hu], and GAD65 antibody); 22 patients, for neural PMP receptor or ion channel antibodies (most commonly targeting P/Q- or N-type voltage-gated calcium channels); and 15 patients, for antibodies from both categories. Neurologic improvements occurred in 54 patients (with a robust change in ambulatory ability in 22) attributable to immunotherapy; univariate regression analysis revealed that improvements were significantly more common among patients with nonparaneoplastic disorders (P = .03) and those with exclusively PMP antibodies (P = .02). Kaplan-Meier analyses revealed that progression to wheelchair dependence occurred significantly faster among patients with NNC antibody positivity only (P = .02), although those with GAD65 autoimmunity progressed to wheelchair dependence at a rate similar to those with PMP autoimmunity (P = .92). CONCLUSIONS AND RELEVANCE: Although autoimmune ataxia is usually severe, treatment responses can be gratifying, particularly in patients with nonparaneoplastic disorders and in those harboring autoantibodies directed against GAD65 or neural PMPs.

Paraneoplastic cerebellar degeneration as the first evidence of malignancy: a case report.

Paraneoplastic cerebellar degeneration (PCD) is an immune-mediated paraneoplastic disorder affecting the cerebellum. PCD associated with ovarian malignancy is a rare occurrence with fewer than 100 cases reported in published work. PCD patients express anti-Yo antibody, one of the anti-onconeuronal antibodies which is most likely associated with gynecologic or breast malignancies. In this report, we present the case of a 65-year-old postmenopausal woman presenting with acute symptoms of PCD as a first sign of ovarian malignancy.

Gross cerebellar paraneoplastic neurological disorder in a patient with an occult breast cancer.

Paraneoplastic neurological disorders are relatively rare conditions posing both diagnostic as well as therapeutic challenges. A previously fit 66-year-old woman presented with subtle cerebellar symptoms which progressed rapidly over the course of days. Chest x-ray and routine blood tests were unremarkable. CT of the head with contrast showed no abnormality. Lumbar puncture showed no evidence of infection or oligoclonal bands. She was transferred to a neurological centre from a remote and rural setting. Subsequent MRI was reported to be normal as well. Tumour markers were negative but the paraneoplastic anti-Yo antibody was positive. A whole body CT scan revealed a spiculated left breast lesion which turned out to be malignant on fine needle aspiration. She underwent left mastectomy, had plasmapharesis and received high-dose intravenous Ig for her paraneoplastic neurological symptoms. She remained neurologically stable and underwent rehabilitation in her local hospital before getting discharged home.