Bilateral Basal Ganglia Calcification Research Articles

Fahr’s syndrome presenting as focal seizures in an adolescent: a case report

Fahr’s syndrome refers to a rare syndrome which is characterized by symmetrical and extensive intra-cranial calcification. It mostly presents in age group 30-40 years or in older adults, although few cases have also been reported in paediatrics. The usual presentation is in the form of movement disorders, cognitive impairment, neuro-psychiatric manifestations etc. Here we report a case of a 14-year-old adolescent male who came to us with complaints of chronic headache and recurrent episodes of focal seizures. His cranial radio-imaging revealed bilateral basal ganglia calcification. On metabolic workup, he was found to have hypocalcemia and secondary hyperparathyroidism, thus confirming the diagnosis of Fahr’s syndrome.

INTERRELATION BETWEENCARDIAC CONDUCTION ANOMALIES AND RADIOLOGICALFEATURES OF FAHRS SYNDROME: AFACT OR COINCIDENCE? CASE REPORT AND REVIEW OF THE LITTERATURE

Introduction:Fahrs syndrome is a rare, slowly progressive, neurodegenerativedisorder, characterized by extensive, bilateral, and symmetrical basal ganglia calcification. It isassociatedwithneuropsychiatric manifestations and gradually progressive cognitive impairment. Fahrs syndrome is the secondaryform of brain calcification thatiscaused by variousmetabolic, infectious, or degenerativediseases. Case report:An old manwasadmittedto ourdepartmentwithrecurrentepisodes of syncope. An electrocardiogramrevealedcomplete AV block.Laboratoryresultsdisclosedhypocalcemia, pseudo hypoparathyroidism, and hyperphosphatemia. Computedtomographyrevealedintracranial calcifications suggestiveofFahrs syndrome. Conclusion:Fahrs syndrome is a rare anatomo-clinical and radiologicalentity, with multiple clinical and etiological aspects. The pathophysiologicalmechanism of the lesionsremainspoorlyunderstood, even more cardiacfeaturesthatmaycause, but is set to benefitfromadvances in functionalneuroimaging.

MT-TN mutations lead to progressive mitochondrial encephalopathy and promotes mitophagy

Mitochondrial encephalopathy is a neurological disorder caused by impaired mitochondrial function and energy production. One of the genetic causes of this condition is the mutation of MT-TN, a gene that encodes the mitochondrial transfer RNA (tRNA) for asparagine. MT-TN mutations affect the stability and structure of the tRNA, resulting in reduced protein synthesis and complex enzymatic deficiency of the mitochondrial respiratory chain. Our patient cohort manifests with epileptic encephalopathy, ataxia, hypotonia, and bilateral basal ganglia calcification, which differs from previously reported cases. MT-TN mutation deficiency leads to decreased basal and maximal oxygen consumption rates, disrupted spare respiratory capacity, declined mitochondrial membrane potential, and impaired ATP production. Moreover, MT-TN mutations promote mitophagy, a process of selective degradation of damaged mitochondria by autophagy. Excessive mitophagy further leads to mitochondrial biogensis as a compensatory mechanism. In this study, we provided evidence of pathogenicity for two MT-TN mutations, m.5688 T > C and m.G5691A, explored the molecular mechanisms, and summarized the clinical manifestations of MT-TN mutations. Our study expanded the genotype and phenotypic spectrum and provided new insight into mt-tRNA (Asn)-associated mitochondrial encephalopathy.

Secondary Fahr’s syndrome mimicking meningoencephalitis

Introduction and aim. Fahr’s disease is a rare neurological disorder characterized by bilateral basal ganglia calcifications. The aim of this report is to highlight a case of Fahr’s disease with atypical features such as neck rigidity and peripheral nerve involvement. Description of the case. Here, we present the case of a South Asian patient with secondary Fahr’s disease whose clinical presentation mimicked that of meningoencephalitis. The patient had neurological and neuropsychiatric symptoms along with abnormal body movements. She also had restricted neck mobility. Computed tomography of the head revealed bilateral dense calcifications in the basal ganglia suggestive of Fahr’s syndrome. Investigations revealed severe hypocalcemia, hyperphosphatemia, and low parathyroid hormone levels, which led to the identification of hypoparathyroidism as the underlying cause. The presence of pre-existing epilepsy and neck rigidity made the diagnosis difficult. The relatively rapid development of symptoms along with the presence of peripheral nerve involvement made this case even more unique. Calcium levels were corrected, and there was a marked symptomatic improvement. Conclusion. Neck rigidity and restricted neck mobility may be present in cases of Fahr’s syndrome due to calcifications of the nuchal ligament or other spinal ligaments and thus must be differentiated from meningoencephalitis. Although the symptoms of Fahr’s syndrome are generally limited to the central nervous system, there may be involvement of the peripheral nerves as well.

A patient with suspect of Fahr syndrome caused by secondary hypoparathyroid after total thyroidectomy

Background: Hypoparathyroid is an endocrine disorder that is characterized by hypocalcemia and hyperphosphatemia due to insufficient secretion of parathyroid hormone. Mostly, this disease is secondary caused by neck surgery and it is responsible for almost all cases of hypoparathyroid. Parathyroid hormones responsibles for maintaining homeostasis of calcium. Fahr syndrome is a neurodegenerative disorder characterized by bilateral basal ganglia calcification that is caused by endocrine disorder such as hypoparathyroid. Case Presentation: In this case report, we reported a 70 years old woman with secondary hypoparathyroidism presenting with Fahr's syndrome after total thyroidectomy. Besides hypocalcemia and hyperphosphatemia as signs of secondary hypoparathyroidism, specific clinical signs with Fahr's syndrome in this case is presence of multiple calcifications in several parts of the brain and specifically in the bilateral of basal ganglia. Management of this disease mainly focused on supplementation of calcium and vitamin D. Conclusion: Fahr syndrome is a rare, genetically dominant, inherited neurological disorder that should be considered as the main problem in several patients with post total thyroidectomy.

Identification of m.3243A>G mitochondrial DNA mutation in patients with cerebellar ataxia

The mitochondrial DNA m.3243A>G mutation can affect mitochondrial function and lead to a wide phenotypic spectrum, including mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, diabetes mellitus, hearing impairment, cardiac involvement, epilepsy, migraine, myopathy, and cerebellar ataxia. However, m.3243A>G has been rarely reported in patients with cerebellar ataxia as their predominant manifestation. The aim of this study is to investigate the prevalence and clinical features of m.3243A>G in a Taiwanese cohort of cerebellar ataxia with unknown genetic diagnosis. This retrospective cohort study conducted the mutation analysis of m.3243A>G by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) in 232 unrelated Han Chinese patients with genetically-undetermined cerebellar ataxia. The clinical presentation and neuroimaging features of patients with m.3243A>G mutation-related cerebellar ataxia were characterized. We identified two patients harboring m.3243A>G mutation. These patients have suffered from apparently sporadic and slowly progressive cerebellar ataxia since age 52 and 35 years, respectively. Both patients had diabetes mellitus and/or hearing impairment. The neuroimaging studies revealed generalized brain atrophy with predominantly cerebellar involvement in both individuals and bilateral basal ganglia calcifications in one of the patients. Mitochondrial m.3243A>G mutation accounted for 0.9% (2/232) of genetically-undetermined cerebellar ataxia in the Han Chinese cohort in Taiwan. These findings highlight the importance of investigating m.3243A>G in patients with genetically-undetermined cerebellar ataxia.

Symmetrical and bilateral basal ganglia calcification. Case series and literature review

Symmetrical and bilateral basal ganglia calcification. Case series and literature review

Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes with an MT-TL1 m.3243A>G point mutation: Neuroradiological features and their implications for underlying pathogenesis.

Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is one of the most common inherited mitochondrial disorders. Due to the high clinical and genetic heterogeneity of MELAS, it is still a major challenge for clinicians to accurately diagnose the disease at an early stage. Herein, we evaluated the neuroimaging findings of MELAS with an m.3243A>G mutation in MT-TL1 and analyzed the possible underlying pathogenesis of stroke-like episodes. Fifty-nine imaging studies in 24 patients who had a confirmed genetic diagnosis of m.3243A>G (MT-TL1; tRNA Leu) associated with MELAS were reviewed in our case series. The anatomic location, morphological features, signal/intensity characteristics and temporal evolution of lesions were analyzed on magnetic resonance imaging (MRI), and computed tomography (CT) images. The supplying vessels and metabolite content of the lesions were also evaluated by using MR angiography (MRA)/CT angiography (CTA), and MR spectroscopy (MRS), respectively. The lesions were most commonly located in the posterior brain, with 37 (37/59, 63%) in the occipital lobe, 32 (32/59, 54%) in the parietal lobe, and 30 (30/59, 51%) in the temporal lobe. The signal characteristics of the lesions varied and evolved over time. Bilateral basal ganglia calcifications were found in 6 of 9 (67%) patients who underwent CT. Cerebral and cerebellar atrophy were found in 38/59 (64%) and 40/59 (68%) patients, respectively. Lesion polymorphism was found in 37/59 (63%) studies. MRS showed elevated lactate doublet peaks in 9/10 (90%) cases. MRA or CTA revealed that the lesion-related arteries were slightly dilated compared with those of the contralateral side in 4 of 6 (67%) cases. The imaging features of MELAS vary depending on the disease stage. Polymorphic lesions in a single imaging examination should be considered a diagnostic clue for MELAS. Stroke-like episodes may be involved in a complex pathogenetic process, including mitochondrial angiopathy, mitochondrial cytopathy, and neuronal excitotoxicity.

SLC20A2-Associated Idiopathic basal ganglia calcification (Fahr disease): a case family report

BackgroundIdiopathic basal ganglia calcification (IBGC) is a genetic disorder of the nervous system commonly known as Fahr disease. IBGC patients with a genetic background are considered to have primary familial brain calcification (PFBC), also known as familial basal ganglia calcification (FBGC), or familial Fahr disease. It is a rare degenerative neurological disorder characterized by extensive bilateral basal ganglia calcification that can lead to a range of extrapyramidal symptoms and neuropsychiatric manifestations. Studies have suggested that more than 50 variants of SLC20A2 gene mutations account for approximately 50% of IBGC cases. There is a wide spectrum of mutation types, including frameshift, nonsense, and splice site mutations in addition to deletion and missense mutations. Here we report a case of familial basal ganglia calcification caused by a frameshift mutation in the SLC20A2 gene. We identified a heterozygous mutation in the SLC20A2 gene, c.1097delG (p.G366fs*89). To our knowledge, this mutation site has not been reported before.Case presentationA 57-year-old male patient was admitted to the hospital with “unstable walking and involuntary movements between the eyes and eyebrows for 6 months”. Based on the patient’s family history, symmetrical calcification foci in the bilateral caudate nucleus head, thalamus, cerebellum and parietal lobe indicated by head CT, and gene test results, the diagnosis of familial Fahr disease caused by mutations in the SLC20A2 gene, c.1097delG p.G366fs*89) was confirmed.ConclusionFor the first time, we identified c.1097delG (p.G366fs*89) as a frameshift mutation in the IBGC family. This frameshift mutation caused the condition in this family of patients. This mutation not only broadens the range of known SLC20A2 mutations but also aids in the genetic diagnosis of IBGC.

Seizures and bilateral basal ganglia calcifications due to hypoparathyroidism after thyroidectomy

Seizures and bilateral basal ganglia calcifications due to hypoparathyroidism after thyroidectomy

SLC20A2-related primary familial brain calcification with purely acute psychiatric symptoms: a case report

BackgroundPrimary familial brain calcification (PFBC) is a rare inherited neurological disorder characterized by bilateral basal ganglia calcification with a series of motor and nonmotor symptoms. Mutations in the SLC20A2 gene, encoding the PiT2 protein, are the major cause of the disease. Here, we report a Chinese PFBC family carrying a SLC20A2 gene mutation, and the proband presented with purely acute psychiatric symptoms, which has been rarely reported in this disease.Case presentationA 38-year-old woman was hospitalized due to disorganized speech; disordered thought contents; disorganized behaviour; emotional instability and lability; and grandiose words, actions and facial expressions. Brain computerized tomography (CT) revealed calcification in the basal ganglia; cerebellar dentate nuclei; and subcortical, periventricular, and deep white matter regions in she and her family members. Through mutation analysis, a heterozygous truncating mutation, c.1723G > T, p.(Glu575*), was identified in the SLC20A2 gene in this family. Thus, this patient was diagnosed with genetically confirmed PFBC, and she responded well to a low dose of antipsychotic drugs. The penetrance of the disease in this family was only 33%, which was significantly lower than that in most families carrying SLC20A2 gene mutations.ConclusionsPatients with SLC20A2-related PFBC might present with psychiatric symptoms alone, and the penetrance of the disease may be quite low, which adds to the clinical heterogeneity of the disease.

A Case of Pseudohypoparathyroidism - Rarely Encountered in Clinical Practice

Physiological intracranial calcification occurs in about 0.3-1.5% of cases. It is asymptomatic and detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases. Hypoparathyroidism and pseudohypoparathyroidism are the one of the causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders. Fahr’s syndrome is a rare entity characterized by the presence of bilateral intracranial calcifications with predilection for the basal ganglia and dentate nuclei. It is commonly associated with endocrine disorders, particularly parathyroid and Vitamin D disturbances. Herein we report a case of pseudohypoparathyroidism revealed by Fahr’s disease.

Mineralizing angiopathy with basal ganglia stroke after minor head trauma; a clinical profile and follow up study of a large series of paediatric patients from North India.

There is paucity of published literature on follow-up outcome of mineralizing angiopathy with basal ganglia stroke related to minor head trauma. This retrospective study aims to bridge this knowledge gap. Patients (1 months- 15 years), presenting with acute stroke over a 5-year period were recruited. From this cohort, basal ganglia strokes following minor head trauma were analysed in detail and outcome assessed using the Recovery and Recurrence Questionnaire (RRQ). A total of 94 patients were eligible, 48 (51%) were basal ganglia stroke following minor head trauma [M: F 2.5:1; mean age 21±8.5 (±SD months]. Further evaluation of this group revealed a median time of 60min (range 0-96h) from trauma to stroke onset. Nearly all had acute hemiparesis (45/48). Almost a third of patients (n=13; 27%) had a transient hemi dystonia on the hemiparetic side after a median of 4 days (range 2-6 days) of symptom onset.Computed tomography (CT) head showed bilateral basal ganglia calcification in all; Most patients (31/48; 64.5%) were anaemic. Magnetic Resonance (MR) angiography, echocardiogram and thrombophilia screen was normal wherever they were performed (6/48).The median follow-up period - 14 months (Range 0-22months). Majority of patients (22/35; 63%) showed complete recovery at 18 months follow up, with maximum recovery occurring between 6 and 12 months. Minor head trauma leading to basal ganglia stroke in children was the most common cause of paediatric stroke in our patients. In follow-up most patients had recovered fully, though a significant minority did not recover completely.

A Case of Psychosis Due to Acute Hypocalcemia From Hypoparathyroidism

A 61-year-old female with past medical history of depression, hypoparathyroidism (hypoPtH), and hypothyroidism had disappeared from her home and was found wandering a few hours away with persecutory delusions, visual and auditory hallucinations. Serum calcium (Ca) was 6.3 mg/dL (range 8.6–10.2), albumin 3.7 g/dL (range 3.5–5.2) and ionized Ca 0.89 mmol/L (range 1.12–1.30). She was admitted and treated with Ca and calcitriol. Work-up for altered mental status was negative except for hypocalcemia (hypoCa) and scattered bilateral basal ganglia calcifications (BGC) with cortical and subcortical frontal lobe calcifications on CT. Psychiatry diagnosed delirium due to hypoCa. Acute psychosis resolved once Ca levels improved. Diagnosis of idiopathic hypoPtH was in 1997. Her regimen included Ca citrate 1500mg daily and 10 mcg of Forteo twice daily. She had skipped her medications for at least 2 days prior to presentation.Her medical records revealed that she was seen for severe depression, progressive gait abnormalities, slowed movements, and imbalance, in 2015. CT scan and MRI brain showed BGC. Her son gave a history of multiple admissions for psychosis, violence, delusions with agitation, and wandering at times when the patient was hypoCa, which was diagnosed as schizophrenia. Neuropsychiatric disturbances are commonly associated with hypercalcemia. Review of literature found a few case reports of psychosis and hypoPtH 1,2 BGC is common in hypoPtH. Psychotic symptoms due to BGC include auditory hallucinations, delusions of influence, paranoid states, and complex perceptual distortions.3,5 HypoCa is associated with cognitive impairment. Neurological manifestations tend to improve with Ca correction, but psychiatric symptoms do not improve substantially.4,5 Further studies are needed in hypoPtH with BGC to appropriately diagnose organic psychosis. This is important in management of the vicious cycle of psychiatric illness leading to noncompliance resulting in psychosis. Prevention of BGC will play a key role.

Bilateral Basal Ganglia Calcification; An Unusual Initial Presentation of Pseudohypoparathyroidism

Physiological intracranial calcification occurs in about 0.3–1.5% of cases. Hypoparathyroidism and pseudohypoparathyroidism are the most common causes of pathological basal ganglia calcification.A 21-year-old female who was initially evaluated by neurology team for headache and diplopia, underwent MRI of brain which revealed Calcifications involving the bilateral basal ganglia, thalami, dentate nuclei as well as juxtacortical frontal lobes. She reported Fatigue and muscle pain, usually in her arms especially after playing sports which had been going on for many years. She had no history of fractures, seizures, psychiatric disorders, developmental delay or obvious cognitive impairments. She denied any family history of calcium disorders or autoimmune diseases. As she had been generally healthy in her whole life, she never had any lab testing done. On examination, Height 5’1”, Chvostek’s sign was positive. Fundoscopy was normal. she had no dysmorphic features or shortened 4th metacarpal. Investigations revealed serum calcium less than 5.0 mg (N 8.3 - 10.1 mg/dl), PTH 205.1 pg/ml (N 18.4 - 80.1 pg/ml), phosphate 7.1 mg (N 2.5 - 5 mg), Vitamin-D 36.2 ng/ml (N 30.0 - 100.0 pg/ml),magnesium 2.0 m (N 1.6 - 2.6 mg/dl) with normal albumin, alkaline phosphatase and renal function test. She was diagnosed with pseudohypoparathyroidism and started on calcium and active vitamin D supplement and was referred for genetic testing study. She reported significant improvement in myalgia after a few weeks of starting calcium and active vitamin D supplementations and repeat lab testing showed improved hypocalcemia and hyperphosphatemia. This case illustrates unusual presentation of PTH resistance with basal ganglia calcification as initial presentation prompting further workup. She likely has pseudohypoparathyroidism type 1b.Since adequate treatment of hypoparathyroidism may lead to marked clinical improvement, determination of serum calcium, phosphorus, and parathyroid hormone is mandatory in all individuals with calcification of the basal ganglia to rule out hypoparathyroidism.

Fahr’s syndrome due to hypoparathyroidism revisited: A case of parkinsonism and a review of all published cases

IntroductionFahr’s syndrome due to hypoparathyroidism refers to bilateral basal ganglia (BG) calcifications and manifests with movement disorders, seizures, cognitive and behavioral symptoms. Case presentationWe report a case of a 74-year-old woman, who presented with parkinsonism due to post-surgical hypoparathyroidism and normal DaT scan, despite extensive calcifications of the BG, periventricular white matter, and cerebellum. MethodsA comprehensive literature review of all reported cases of Fahr’s syndrome due to hypoparathyroidism was conducted in the electronic databases PubMed and Web of science. Moreover, demographic and clinical characteristics of the patients overall were calculated and associated with radiological findings. ResultsWe reviewed a total of 223 cases with Fahr’s syndrome due to hypoparathyroidism (124 female, 99 male). Mean age on presentation was 44.6 ± 17.7 years. Thirty nine percent of patients had idiopathic hypoparathyroidism, 35.4 % acquired and 25.6 % pseudohypoparathyroidism. Almost half of the patients had tetany, seizures or a movement disorder and approximately 40 % neuropsychiatric symptoms. The patients with a movement disorder had a 2.23 likelihood of having neuropsychiatric symptoms as well (OR 2.23, 95 % CI 1.29–3.87). Moreover, there was a statistically significant association between the phenotype severity (i.e. the presence of more than one symptom) and the extent of brain calcifications (χ2 = 32.383, p = 0.009). ConclusionFahr’s syndrome is a rare disorder, which nonetheless manifests with several neurological symptoms. A head CT should be considered for patients with hypoparathyroidism and neurological symptoms. More studies using DaT scan are needed to elucidate the effects of calcifications on the dopaminergic function of the BG.

Fahr’s syndrome in teenage girls with systemic lupus erythematosus: A case report

Fahr’s disease or Fahr’s syndrome is a condition characterized by intracranial calcifications especially in basal ganglia and dentate nuclei. They are a rare condition with a broad range of manifestations from asymptomatic condition to severe neurological and psychiatry signs and symptoms. The aim of this report to present Fahr’s syndrome as an alternative diagnosis of neuropsychiatry symptoms in systemic lupus erythematosus (SLE) patients. We present a 17-year-old teenage girl who have had a preexisting diagnosis of SLE and have been on remission. The patient recently had experienced headache, auditory hallucination and memory loss despite having a low activity score of SLE and no laboratory relapse. Head CT scan showed bilateral basal ganglia calcifications suggesting a Fahr’s disease. Clinical outcome in this condition might vary but might worsen neurocognitive functions.

A rare consortium of functional neurological disorder and Fahr’s disease - a herald of extensive calcification

Fahr’s disease is also known as familial idiopathic basal ganglia calcification affecting the cerebral microvessels and presenting with numerous neuropsychiatric manifestations. Functional neurological disorder (FND), a pure neuropsychiatric phenomenon occurs rarely in Fahr’s disease. Herein, we have presented a case of 17 year old female presenting neuropsychiatric symptoms like pseudoseizure, left sensorineural deficit and mild headache for last 4 months. Mental status examination revealed impaired attention and concentration. Laboratory examinations were within normal limits except CT scan and MRI Brain which revealed bilateral and symmetrical basal ganglia calcification. This is a rare case of FND associated with Fahr’s Disease, never reported in the literature. This case highlights the need for evaluating the biological factors in causation of FND where psychological factors were not assessed.

Fahr’s Syndrome and Pseudohypoparathyroidism- A rare clinical entity

Physiological intracranial calcification occurs in about 0.3-1.5% of cases. It is asymptomatic and detected incidentally by neuroimaging. Pathological basal ganglia calcification is due to various causes, such as: metabolic disorders, infectious and genetic diseases. Hypoparathyroidism and pseudohypoparathyroidism are the one of the causes of pathological basal ganglia calcification. Besides tetany and seizures this condition is presented by parkinsonism and dementia. Infections (toxoplasmosis, rubella, cytomegalovirus, cysticercosis, AIDS) give multiple and asymmetric intracranial calcification. Inherited and neurodegenerative diseases cause symmetrical, bilateral basal ganglia calcification which is not related to metabolic disorders. Fahr’ssyndrome is a rare entity characterized by the presence of bilateral intracranial calcifications with predilection for the basal ganglia and dentate nuclei. It is commonly associated with endocrine disorders, particularly parathyroid and Vitamin D disturbances. Herein we report a case of pseudohypoparathyroidism revealed by Fahr’s disease.

Fahr´s disease presenting with epileptic seizures: a case report

Fahr is a rare neurological disorder that leads to abnormal, symmetrical, and bilateral calcification of the basal ganglia and other brain regions, seizures are one of many symptoms to lead to the diagnosis of this disease. We here report a 45-year-old male diagnosed as Fahr´s disease presenting with loss of consciousness and multiples seizures. A 45-year-old male with a history of an untreated depressive syndrome, smoking, and active alcoholism, admitted to the emergency department with a sudden loss of consciousness and multiples seizures. The Computed tomography scan showed a bilateral and symmetric deposit of calcifications in basal ganglia, the blood tests excluded any other anomaly that may lead to secondary intracranial calcification, the patient denied any similar cases in the family, the clinical, biological and radiological findings were compatible with a sporadic form of Fahr´s disease. Seizures are ones of the rarest symptoms that can reveal a Fahr´s disease, the finding of bilateral and symmetrical calcification of basal ganglia in a patient presenting with seizures should be reminiscent of this illness after excluding any other pathological processes leading to secondary intracranial calcification.