<p>  </p> <p>Disfluencies are a commonly reported speech symptom associated with Parkinson disease (PD), though the cause remains unknown. Studies have consistently reported that people with PD experience more disfluencies, particularly atypical disfluencies compared to healthy controls. One proposed theory, known as the dualistic model of dopamine levels and stuttering, posits that abnormally high or low levels of dopamine may cause an increase in disfluencies. The aim of the current study is to examine how levodopa medication and deep-brain stimulation affect fluency in people with PD. Twenty-seven participants with PD underwent testing before (on and off medicine) and six months after deep-brain stimulator implant surgery (optimally medicated, on and off stimulation). Participants read a passage aloud and provided a 2-minute monologue. Speech samples were transcribed. The number of typical and atypical disfluencies were identified auditorily and using a wide-band spectrogram. After surgery, most participants reduced their levodopa equivalency dose from pre-implant levels. Results demonstrated no significant differences in frequency of disfluencies across time (pre-surgery, post-surgery) or condition (on/off medication/stimulation). Overall, participants produced more typical than atypical disfluencies and more disfluencies in the monologue task than the reading task. Results do not support the dualistic model of dopamine, but instead support a more nuanced and individualized role for dopamine in speech fluency. For example, patterns within individual subjects suggest changes in dopamine may play a role in speech fluency for individual patients with PD. Data support the effect of cognition and language formulation in the production of disfluencies, particularly typical disfluencies.</p>

<p dir="ltr">Papilledema is the swelling of the optic disc resulting from increased cranial pressure. The diagnosis of papilledema is important not only to treat pathologies of the eye, but it also can be an important indicator for underlying brain pathology since the subarachnoid space surrounding the optic nerve is contiguous with the brain. Therefore increased pressure from the brain from pathologies such as hydrocephalus can be transmitted to the posterior eye. To study papilledema, a reproducible post hemorrhagic hydrocephalic rat model was used to study the changes of the retina, optic disc and optic nerve when exposed to high intracranial pressure. Multiple changes were noted in the post hemorrhagic hydrocephalic model including decreased thickness of the ganglion cell complex, decreased retinal thickness in the periphery in females, increased retinal thickness close to the optic nerve in males, increased optic disc width and diameter along with a decrease number of retinal ganglion cells. These findings were similar to findings in human patients with papilledema. Therefore, future studies are indicated using the post hemorrhagic hydrocephalic rat model to further understand the mechanism of papilledema progression and the use of possible therapeutics.</p>

Tension-Type Headache (TH) is highly prevalent and associated with significant personal and social cost. The causes of TH are unclear, precluding optimal treatment or prevention at present. Stress is a well-documented correlate and trigger of TH activity, however the causal significance has not been experimentally demonstrated to date. Similarly, the mechanisms by which stress contributes to TH, if in fact it does, are not clearly understood. Findings of increased pain sensitivity in TH sufferers suggests TH pathophysiology may involve dysfunction in peripheral and/or central nervous system processing of pain. Studies on animals and healthy humans demonstrate that stress can increase pain sensitivity by affecting peripheral and central pain mechanisms proposed as dysfunctional in TH. It has therefore been proposed that stress may contribute to TH through aggravating already increased pain sensitivity in TH sufferers. However, this hypothesis has not been adequately examined in TH sufferers to date. Addressing the above issues, the present project conducted seven studies examining relationships between stress, pain sensitivity, and headache activity in TH sufferers. The aim was to test the hypothesis that stress contributes to TH by aggravating already increased pain sensitivity in TH sufferers. Studies 1 and 2 demonstrated increased general arousal and complex temporal relationships between general arousal and headache activity in the natural environment in Episodic TH (ETH) sufferers. In Study 3, experimentally induced stress of brief duration increased pressure pain sensitivity at the head in Chronic TH (CTH) sufferers more than in healthy controls. Study 4 found CTH sufferers to have increased levels of daily stress, increased pericranial muscle tenderness, and reduced pain thresholds, which were inter-related. Both daily stress and pain sensitivity were predictive of prospective daily headache activity. In Study 5, an experimental model demonstrated that stress-induced headache was associated with stress-induced increase in pericranial muscle tenderness and reduction in pressure pain thresholds at head and hand. Additionally, induced stress reduced pain tolerance and increased pain intensity ratings to cold pressor more in TH sufferers than in healthy controls (Study 7). Finally, TH sufferers were found to have abnormal temporal summation of pressure pain and impaired noxious inhibition of temporal summation compared to healthy controls, however neither temporal summation nor noxious inhibition of temporal summation were affected by induced stress (Study 6). Together, the results support the hypotheses: 1) Stress contributes to both ETH and CTH, and 2) Stress contributes to CTH through aggravating already increased pain sensitivity in CTH sufferers. Impaired pain inhibition and increased wind-up may be underlying abnormalities contributing to increased pain sensitivity in CTH sufferers.