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Introduction. Paraneoplastic neurological syndromes (PNS) refer to a diverse group of nervous system disorders associated with tumors. They are not directly caused by a tumor’s immediate expansion, compression resulting from it, infiltration or anticancer treatment. Their pathomechanism involves damage to the nervous system as a result of the organism’s immune response directed against cancer antigens, and also against antigens occurring physiologically in the nervous system. Onconeural antibodies and cytotoxic T lymphocytes are responsible for the immune response. These conditions are quite rare - fewer than 1 person out of 100 patients suffering from cancer develops PNS. They often precede a direct manifestation of cancer. The best known PNS conditions include: Lambert-Eaton myasthenic syndrome, paraneoplastic cerebellar degeneration, and polyneuropathies. PNS was identified for the first time in 1949. Nowadays, the criteria established in 2004 by Graus et al. have been followed in diagnostics. These define the conditions for arriving at a possible and definite diagnosis based on the presence of a characteristic neurological syndrome, the presence of onconeural antibodies, and detecting neoplasm before or after the manifestation of neurological symptoms. Diagnosis is difficult due to the lack of laboratory markers (onconeural antibodies are present in serum only in 50-60% of cases) or direct cancer symptoms in the first phase of the disease. Aim. This paper aimed at recounting the existence of a very rare neurological syndrome, limbic encephalitis, which can develop in the course of a neoplastic disease. Awareness of PNS and detecting neoplasm beforeits direct clinical manifestation can contribute to a better prognosis for patients.Materials and methods. This paper is based on a case analysis concerning a patient manifesting symptoms of the limbic system involvement. The medical history has been interpreted, additional examination results have been analyzed, and the developing clinical manifestations have been investigated. Case study. The presented patient is a 45-year old man in whose case limbic encephalitis exceeded detecting abdominal cancer by a year. Diagnostic difficulties were caused by a synchronous pituitary microadenoma and hormonal disturbances involving cortisol and prolactin, which suggested Cushing’s syndrome. The main clinical symptoms, intensifying in time during the course of the disease lasting several months included: recent memory disturbances, allopsychic disorientation, depression, and periodical aggression. Results and discussion. Conducted serum tests to screen for onconeural antibodies did not confirm their presence. However, a magnetic resonance imaginig (MRI) scan revealed bilateral hippocampal damage. On the basis of a typical clinical syndrome, and cancer identified after a year following the occurrence of the symptoms, a definite, according to Graus’ criterion, diagnosis of PNS was established. Conclusions. Awareness and knowledge of PNS contributes to an early diagnosis and detection of cancer. This creates an opportunity to introduce adequate treatment and improves the prognosis for the patient. [ABSTRACT FROM AUTHOR]

Introduction. Acute liver porphyrias are caused by mutations of genes encoding the heme biosynthesis enzymes. A lack of any of these enzymes leads to a decrease in the heme level, which in each case is manifested by identical clinical symptoms. Nervous tissue is particularly susceptible to a depletion of heme levels. Three classical symptoms of a porphyria attack include: abdominal pain (as a manifestation of autonomic neuropathy), peripheral neuropathy, and psychic disturbances. Apart from the main symptoms, porphyria attacks may be manifested as various neurological disturbances, such as: bulbar palsy, epileptic seizures, psychic disturbancesand focal symptoms of CNS damage. The intensity of individual symptoms can vary. Although neurological symptoms usually disappear after the attack, they may cause permanent deficits. Through involving CNS, porphyria can mimic other neurological disorders. Damage to the nervous system can be confirmed by additional examinations. Thus far, disseminated focal changes during the attack, which disappear after the regression of clinical symptoms, have been described in magnetic resonance imaging (MRI) scans of the brain. Spinal cord abnormalities in MRI scans have not been described yet, despite the fact that damage to the anterior horn associated with porphyria has been confirmed in literature. While examining cerebrospinal fluid during the attack, an elevated protein level has been noticed, so far without the presence of oligoclonal bands. Aim. This paper aimed to demonstrate that porphyria should be considered in differential diagnosis of clinically isolated syndrome (CIS) and multiple sclerosis (MS). Materials and methods. This paper is based on the case of a symptomatic patient who carried a mutation in one of the genes for porphyria, and who developed a clinical manifestation of focal damage to CNS. A differential diagnosis of porphyria and CIS, with a subsequent conversion to a clinically defined MS, was carried out. The results of additional examinations performed routinely in both disorders, the clinical picture and data from medical literature have been used in the analysis of this case. Case study. The authors present the case of a patient with confirmed genetic porphyria, who was hospitalized for purposes of establishing a diagnosis due to weakened lower extremities. The patient manifested spastic lower extremity paresis, sensation disorders and urinary incontinence, which indicated spinal cord damages. An MRI scan of the thoracic spine revealed disseminated foci with contrast enhancement. A high level of proteins and oligoclonal bands were detected in the cerebrospinal fluid. On the basis of a new clinical picture (differing from the previous attack symptoms), prolonged symptoms, spinal cord lesions in MRI, and the presence of oligoclonal bands, CIS was diagnosed. Quick and complete recovery was obtained due to the administering of a steroid therapy. After several months, the patient reported a similar, passing episode, which, according to the authors, confirmed the diagnosis and an expected conversion to a clinically defined MS. Results and discussion. Taking into consideration the clinical manifestation of spinal cord involvement untypical of porphyria, the detection of spinal lesions in an MRI scan, the presence of oligoclonal bands in the cerebrospinal fluid and the positive effect of steroid therapy, the authors believe that this described patient, who was a symptomatic carrier of a mutation in a gene for porphyria, developed CIS. Conclusions. This reported case, supported by data from medical literature, shows that porphyria should be taken into consideration in any differential diagnosis of CIS and MS. [ABSTRACT FROM AUTHOR]

Introduction. An epidermoid cyst (EC) is a congenital, benign, and nonifiltrating tumor which originates from the central nervous system (CNS) as a result of neural tube defects (NTD). The presence of lesion may cause CNS symptoms by means of mass-effect, when compressing the adjacent structures, or rupture and secondary aseptic inflammatory process. Within the CNS, EC is most frequently located in: pontocerebellar angle, suprasellar region, posterior cranial cavity, and spinal canal. The clinical symptoms can be general, like headache or dependent on the lesion location: dizziness, nystagmus, damage to the cranial nerves within the pontocerebellar angle and brain stem, disturbed fields of vision, and epileptic seizures. Magnetic resonance imaging (MRI) allows for visualizing the lesion which is shown as a heterogenic iso- or hypointense mass in relation to the cerebrospinal fluid. Using diffusion weighted images (DWI) is a helpful tool in differentiating tumor mass from cerebrospinal fluid. In computed tomography (CT) scans, EC has the same or almost the same density as the cerebrospinal fluid which makes the image difficult to differentiate from an arachnoid cyst. Treatment of choice is to remove the lesion in a possibly complete spectrum. In asymptomatic patients or patients exhibiting a mild intensity of symptoms, it is possible to wait and observe which solution could be chosen. Aim. The aim of this paper was to present a case report concerning treatment of an EC located in the craniovertebral junction. Materials and methods. A clinical management concerning a patient diagnosed and treated both in an outpatient clinic and in hospital at the departments of neurology and neurosurgery has been described. Case study. A 69-year old female patient came to the Neurology Outpatient Clinic complaining of headaches, pain in her neck, and balance disturbances. These symptoms had intensified for 2 years. An MRI scan of the cervical spine revealed a large lesion in the posterior cranial cavity. An MRI scan of the head showed a multicystic tumor located in the posterior fossa in the projection of cerebellomedullary cistern, which did not undergo contrast intensification. The patient was treated surgically. Following surgery, headaches, pain in the neck as well as neurological symptoms subsided. Results and discussion. Microsurgical removal of the lesion is the treatment of choice for EC. A total removal should be strived for, preferably en block, although leaving part of the cyst is not a mistake. Postoperative mortality may reach 8.9%, whereas recurrences amount to 4.5% during an 8-year long observation period. EC untreated surgically can, through dermal fistulas, cause bacterial meningitis. Thus, treatment limited to the observation of the lesions may pose a threat, and surgical treatment should be decided upon quickly. Conclusions. Surgical treatment with the use of microscopic technique aided with neuromonitoringallows for removing tumors of the cholesteatoma type safely and radically. [ABSTRACT FROM AUTHOR]