Respiratory dysfunctions have been associated with Parkinson’s disease since the first observations of the disease in 1817. Patients with Parkinson’s disease frequently present respiratory disorders with obstructive ventilatory patterns and restrictive modifications, as well as limitations in respiratory volumes. In addition, respiratory impairments are observed due to the rigidity and kyphosis that Parkinson’s disease patients experience. Subsidiary pulmonary complications can also appear as side effects of medication. Silent aspiration can be the cause of pneumonia in Parkinson’s disease. Pulmonary dysfunction is one of the main factors that leads to the morbidity and mortality of patients with Parkinson’s disease. Here, we performed a narrative review of the literature and reviewed studies on dyspnea, lung volumes, respiratory muscle function, sleep breathing disorders, and subsidiary speech and swallow impairments related to pulmonary dysfunction in patients with Parkinson’s disease.

Cerebral venous sinus thrombosis (CVST) as a severe neurological emergency, is represented by variable conditions in its clinic presentation, onset, risk factors, neuroimagistic features and outcome. The genetic polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene C677T and A1298C was associated with CVST. We aimed to characterize the prevalence of MTHFR gene polymorphisms associated with cardiovascular risk factors in the group of patients with CVST. Also, we studied additional causes associated with CVST including local infections, general infections, obstetric causes (pregnancy, puerperium) and head injury. This is a retrospective study including 114 patients which referred to our hospital between February 2012–February 2020. The protocol included demographic (age, sex), clinical, neuroimagistic features, paraclinic (genetic polymorphism of MTHFR, factor V G1691A—Leiden, prothrombin G20210A, PAI-1 675 4G/5G; Homocysteine level, the lipid profile, blood glucose and Glycohemoglobin HbA1c, high- sensitive C- reactive protein- hsCRP) data, as well as treatment and outcome. The mean age was 37.55 years with a female predominance (65.79%). In the first group of patients with inherited thrombophilia (60 cases; 52.63%) we found genetic mutation includes MTHFR C677T (38.59%) and A1298C (14.03%), factor V G1691A- Leiden (15.78%), prothrombin G20210A (2.63%), PAI-1 675 4G/5G (42.98%), and hyperhomocysteinemia (35.08%). At the second group with other etiology of CVST, except thrombophilia, we included 54 patients (47.36%). The most common sites of thrombosis were the superior sagittal sinus (52.63%). Headache was the most common symptom (91.22%) and seizures were the main clinical presentation (54.38%). The MTHFR polymorphism was significantly correlated with higher total cholesterol (TC) (p = 0.023), low- density lipoprotein cholesterol (LDL) (p = 0.008), homocysteine level (tHcy) (p < 0.001). Inside the first group with MTHFR polymorphism we have found a significant difference between the levels of homocysteine at the patients with MTHFR C677T versus MTHFR A1298C polymorphism (p < 0.001). The high-sensitive C-reactive protein (hsCRP) was increased in both groups of patients, but the level was much higher in the second group (p = 0.046). Mortality rate was of 2.63%. Demographic, clinical and neuroimagistic presentation of CVST in our study was similar with other studies on the matter, with a high frequency of thrombophilia causes. MTHFR gene polymorphisms (C677T and A1298C) are increased in prevalence in CVST. PAI-1 675 4G/5G gene mutation seems to be involved in CVST etiology. Plasma C-reactive protein level and hyperhomocysteinemia should be considered as a prognostic factor in CVST.

Cerebral venous sinus thrombosis (CVST), accounting for less than 1% of stroke cases, is characterized by various causes, heterogeneous clinical presentation and different outcome. The plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms has been found to be associated with CVST. The aim of this retrospective study was to determine the potential association of PAI-1 675 4G/5G polymorphisms and homocysteine levels with cardiovascular risk factors in a group of young patients with CVST. Eighty patients with CVST and an equal number of age and sex matched controls were enrolled. The protocol included demographic and clinical baseline characteristics, neuroimagistic aspects, genetic testing (PAI-1 675 4G/5G polymorphisms), biochemical evaluation (homocysteine—tHcy, the lipid profile, blood glucose, glycohemoglobin—HbA1c, high-sensitive C-reactive protein—hsCRP) data, therapy and prognosis. The PAI-1 675 4G/5G gene polymorphisms were significantly correlated with increased homocysteine level (tHcy) (p < 0.05), higher total cholesterol (TC) (p < 0.05), low- density lipoprotein cholesterol (LDLc) (p = 0.05) and high- sensitive C- reactive protein (hsCRP) (p < 0.05) in patients with CVST when compared with controls. From the PAI-1 gene polymorphisms, the PAI-1 675 4G/5G genotype presented statistically significant values regarding the comparisons of the blood lipids values between the CVST group and control group. The homocysteine (tHcy) was increased in both groups, patients versus controls, in cases with the homozygous variant 4G/4G but the level was much higher in the group with CVST (50.56 µmol/L vs. 20.22 µmol/L; p = 0.03). The most common clinical presentation was headache (91.25%), followed by seizures (43.75%) and focal motor deficits (37.5%). The superior sagittal sinus (SSS) was the most commonly involved dural sinus (56.25%), followed by the lateral sinus (LS) (28.75%). Intima—media thickness (IMT) values were higher in the patients’ group with CVST (0.95 mm vs. 0.88 mm; p < 0.05). The fatal outcome occurred 2.5% of the time. PAI-1 675 4G/5G gene polymorphisms and higher homocysteine concentrations were found to be significantly associated with CVST in young patients.

Cerebral venous and dural sinus thrombosis (CVT) is an uncommon disease in the general population, although it is a significant stroke type throughout pregnancy and the puerperium. Studies describing this subtype of CVT are limited. Most pregnancy-associated CVT happen in late pregnancy, or more commonly in the first postpartum weeks, being associated with venous thrombosis outside the nervous system. Case presentation: The current study describes a case of multiple CVT in a 38-year-old woman with multiple risk factors (including severe inherited thrombophilia and being in the puerperium period), presenting mixed transcortical aphasia (a rare type of aphasia) associated with right moderate hemiparesis and intracranial hypertension. The clinical diagnosis of CVT was confirmed by laboratory data and neuroimaging data from head computed tomography, magnetic resonance imaging, and magnetic resonance venography. She was successfully treated with low-molecular-weight heparin (anticoagulation) and osmotic diuretics (mannitol) for increased intracranial pressure and cerebral edema. At discharge, after 15 days of evolution, she presented a partial recovery, with anomic plus aphasia and mild right hemiparesis. Clinical and imaging follow-up was performed at 6 months after discharge; our patient presented normal language and mild right central facial paresis, with chronic left thalamic, caudate nucleus, and internal capsule infarcts and a partial recanalization of the dural sinuses.

Giant cell arteritis (GCA) is a primary autoimmune vasculitis that specifically affects medium-sized extracranial arteries, like superficial temporal arteries (TAs). The most important data to be considered for the ultrasound (US) diagnosis of temporal arteritis are stenosis, acute occlusions and “dark halo” sign, which represent the edema of the vascular wall. The vessel wall thickening of large vessels in GCA can be recognized by the US, which has high sensitivity and is facile to use. Ocular complications of GCA are common and consist especially of anterior arterial ischemic optic neuropathies or central retinal artery occlusion with sudden, painless, and sharp loss of vision in the affected eye. Color Doppler imaging of the orbital vessels (showing low-end diastolic velocities and a high resistance index) is essential to quickly differentiate the mechanism of ocular involvement (arteritic versus non-arteritic), since the characteristics of TAs on US do not correspond with ocular involvement on GCA. GCA should be cured immediately with systemic corticosteroids to avoid further visual loss of the eyes.