Depression is frequently encountered in Parkinson's disease and was seen to occur in 14 of 26 patients studied. The levels of 5-hydroxyindoleacetic acid (5-HIAA), the main metabolite of serotonin (5-HT), in CSF samples of the patients were significantly lower than in those of controls. However, within the group of patients the levels of 5-HIAA in CSF samples were significantly lower in the depressive subgroup compared with the non-depressive patients. Moreover, no correlation was recorded between motor disability and depression. The results indicate that disturbed 5-HT metabolism may possibly play a role in Parkinson's disease as a predisposing factor in the development of depression.

The aim of this review is to introduce the concept of personalized medicine in secondary stroke prevention with antiplatelet medication. In the last years, many studies have been conducted regarding aspirin resistance and genotyping of clopidogrel metabolism. A review of the currently published data on this issue emphasizes the importance of focusing on the individualizing approach in antiplatelet therapy to achieve maximal therapeutic beneficial effect. However, many authors suggest that, before new information from ongoing trials become available, good clinical practice should dictate the use of low dose of aspirin that was shown to be effective in the prevention of stroke and death in patients with ischemic cerebrovascular disease, because higher doses do not have significantly better efficacy than lower doses in secondary stroke prevention, but lower-dose aspirin is associated with less side effects. On the other hand, many factors are associated with clopidogrel resistance, and recent genetic studies showed that the CYP2C19*2 genotype (loss-of-function allele) is related to poor metabolism of clopidogrel, but larger studies are needed to definitively confirm or rule out the clinical significance of this genetic effect. The aim of personalized approach in secondary stroke prevention is to take the most appropriate medicine in the right dose in accordance with the clinical condition of the patient and associated risk factors.

The American otolaryngologist Eagle was the first to describe styloid syndrome in 1937. Stylohyoid complex is composed of styloid process, stylohyoid ligament and a lesser horn of the hyoid bone. Embriologicaly, these anatomical structures originate from Reichert's cartilage of the second brachial arch. In the general population, the frequency of the elongated styloid process is estimated to be 4%, of which only 4% show clinical manifestations suggesting that the incidence of styloid syndrome is 0.16% (about 16,000 persons in Serbia). The styloid process deviation causes external or internal carotid impingement and pains which radiate along the arterial trunk. Classical stylohyoid syndrome is found after tonsillectomy and is characterised by pharyngeal, cervical, facial pain and headache. Stylo-carotid syndrome is the consequence of the pericarotid sympathetic fibres irritation and compression on the carotid artery. Clinical manifestations are found most frequently after head turning and neck compression. The diagnostic golden standard for styloid syndrome is 3D CT reconstruction. Sagital CT angiography has a leading role in the radiological diagnosis of the stylo-carotid syndrome. Differential diagnosis requires the differentiation of the styloid syndrome from numerous cranio-facio-cervical painful syndromes. If conservative treatment (analgesics, anticonvulsants, antidepressants, and local infiltration with steroids or anaesthetic agents) has no effect, surgical treatment is applied. Styloid syndrome is underrepresented in neurological literature. The syndrome is considered important, because it is clinically similar to many other painful cranio-facial syndromes; it is difficult to be recognized, and the patient should be treated adequately.

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aBackground. Involvement of the central nervous system is registered in a relatively small number of patients with sarcoidosis. In this article we present two cases with various neurological symptoms that fulfill criteria for neurosarcoidosis (NS). In addition, we review the literature on NS with special attention to isolated cranial nerve involvement. Methods and Results. First patient: Neurological examination identified multiple cranial neuropathy, moderate rightsided hemiparesis, polyradiculoneuritis of the lower limbs and positive meningeal signs. Laboratory tests showed serum and cerebrospinal fluid (CSF) inflammatory abnormalities, with increased values of the angiotensin-converting enzyme (ACE). CSF analysis also showed presence of 9 oligoclonal IgG bands. Brain and spine magnetic resonance imaging (MRI) revealed diffuse meningopathy, and focal granulomatous lesion in the body of the L5 vertebra. Lung sarcoidosis was confirmed by additional diagnostic procedures. The patient was treated with Methylprednisolone and a tapering course of oral Prednisone, which reduced the pain in the back and legs and improved the strength of the right leg. However, the other neurological deficiencies remained. After confirming lung sarcoidosis, the patient received Methotrexate in addition to Prednisone but during the following 2 years the patient's condition progressively worsened and ended in death. Second patient: Neurological findings showed weakness of the right n. oculomotorius and the right n. trochlearis, as well as the right-side face weakness. We found raised level of the ACE in serum and CSF. Thorax high-definition computed tomography (HDCTT) showed ribbon-like domains of discrete changes in the pulmonary parenchyma. MRI of the brain showed multiple white matter lesions. This patient also received Methylprednisolone followed by Prednisone, and after two months, ocular motility normalized. Conclusion. The diagnosis of NS is always a challenge. For this rerason definitive diagnosis requires the exclusion of other causes of neuropathy. Multiple cranial neuropathies should always arouse suspicion of NS.