Explore chapters and articles related to this topic
Special considerations: Parkinson’s disease
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Geriatric Neuroanesthesia, 2019
The disease is clinically manifested by three cardinal symptoms: tremor, rigidity, and bradykinesia. The tremor consists of a resting tremor that decreases with purposeful movement. It usually starts unilaterally in the hand and is described as a “pill-rolling” tremor. It is initially intermittent, but as the disease progresses it becomes more frequent and evident. Rigidity is characterized by increased resistance to passive movement. It also usually starts unilaterally, and usually in the same side affected by the tremor. Cogwheel rigidity is an example, and is characterized by a ratchety pattern of resistance and relaxation during a range-of-motion maneuver. Bradykinesia is a generalized slowness of movement and is the most common symptom. Patients may describe it as weakness, feeling unsteady, tiredness, or difficulty performing simple tasks with the hand, such as buttoning clothes.
Impairment of functions of the nervous system
Published in Ramar Sabapathi Vinayagam, Integrated Evaluation of Disability, 2019
Bradykinesia, or paucity of movement, manifests slowing of movement with a progressive decrement in speed or amplitude (36), and the paucity of spontaneous movement. The speech is monotone and hypophonic. Decreased or loss of facial expression, decreased or loss of eye blinking, and mask-like face with or without parted lips present with facial bradykinesia. Persons with bradykinesia may present with drooling of saliva due to impairment of spontaneous swallowing of saliva. Section 4.5.10.1.3.3 in Chapter 4 describes clinical tests to evaluate the severity of bradykinesia. The upper extremity derives maximum impairment of 20% for bradykinesia (Table 6.31) and lower extremity 10% (Table 6.32) and spine 10% (Table 6.33).
Movement Disorders of the Larynx
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Declan Costello, John S. Rubin
Progressive supranuclear palsy (PSP) is a neurological condition that results from accumulations of tau protein in the basal ganglia, brainstem and cerebral cortex. Initial symptoms include loss of balance and bradykinesia. Ocular symptoms such as poor control of eye movements are seen. The speech and laryngeal manifestations in patients with PSP include dysarthria and monotone voice. Treatment is essentially palliative, with l-dopa sometimes providing some control of symptoms.
Optimizing levodopa therapy, when and how? Perspectives on the importance of delivery and the potential for an early combination approach
Published in Expert Review of Neurotherapeutics, 2023
Andrew Lees, Eduardo Tolosa, Fabrizio Stocchi, Joaquim J. Ferreira, Olivier Rascol, Angelo Antonini, Werner Poewe
Up until the mid-1960s, prior to the advent of levodopa therapy, most patients with PD were severely physically disabled or dead within 10 years of disease onset. The only available treatments were anticholinergic drugs and stereotactic thalamotomy, neither of which improved bradykinesia, the most disabling motor symptom of the disease. The magnitude of improvement seen in many patients with levodopa (Larodopa) led to claims, that were not without some justification, that it was a ‘magic bullet’ or ‘miracle drug,’ but its shortcomings and unwanted side effects soon became apparent, leading to adverse publicity that delayed its introduction into clinical practice [7]. Soon after, the combination of levodopa with peripheral dopa decarboxylase (DDC) inhibitors allowed for a fourfold reduction in the dosage of levodopa and a substantial reduction in side effects such as anorexia, nausea, and vomiting [8]. By 1972, Madopar® (levodopa/benserazide) and Sinemet® (levodopa/carbidopa) were the treatment of choice for PD, with anticholinergics and amantadine being used as adjuvant therapy in some patients [9].
The beneficial effect of salubrinal on neuroinflammation and neuronal loss in intranigral LPS-induced hemi-Parkinson disease model in rats
Published in Immunopharmacology and Immunotoxicology, 2022
Fatma Nihan Cankara, Meliha Sümeyye Kuş, Caner Günaydın, Sinan Şafak, Süleyman Sırrı Bilge, Ozlem Ozmen, Emine Tural, Arjan Kortholt
After the apomorphine washout period had passed, animals were tested with rotarod, cylinder, and pole tests. Locomotor activity, motor balance, and skills were evaluated with the rotarod test [23]. Animals were reversely placed on a rotating platform, and latency of the falling was recorded. Before the experiments, the rats were pretrained for 2 days to assure stable performance. On the test day, the rats were placed on an accelerating platform and the falling latencies were recorded. For the cylinder test, the rats were placed in an open plexiglass cylinder (30 × 20 cm) apparatus, and the number of the rearing were recorded. Regularly, rats that are placed in a cylinder will engage in exploratory behavior, including rearing. The times that the animals raise their forelimbs above shoulder level and contact the cylinder wall with each hindlimb were recorded during a 5 min period. The percentage of the use of contralateral limb was calculated according to the total touches [23]. Bradykinesia was assessed with the pole test. The animals were placed on the top of a 1 m long perpendicularly placed metal pole, and the descending time from the pole was recorded [24].
Efficacy and safety evaluation of safinamide as an add-on treatment to levodopa for parkinson’s disease
Published in Expert Opinion on Drug Safety, 2022
Kanako Kurihara, Takayasu Mishima, Shinsuke Fujioka, Yoshio Tsuboi
The diagnosis of PD is based on clinical history and symptoms. The UK Parkinson’s Disease Society Brain Bank clinical diagnostic criteria (UKPDSBB criteria) proposed in 1988 have been widely used [12]. In 2015, new clinical diagnostic criteria were introduced by the Movement Disorder Society (MDS) with the goal to standardize PD diagnosis [13]. While motor symptoms remain the core criteria for PD diagnosis, the importance of non-motor symptoms in diagnosis is also recognized. Bradykinesia and resting tremor or muscle rigidity are the key motor symptoms. The MDS diagnostic framework is comprised of three categories: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow the diagnosis of PD), and supportive criteria (positive features that increase the confidence of PD diagnosis). The diagnostic certainty is then divided into two levels, clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity) [13].