Dementia and Lower Urinary Tract Dysfunction
Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg in Essentials of the Adult Neurogenic Bladder, 2020
Bladder underactivity originates from various causes, including age-related bladder muscle change, and disturbed innervation such as diabetic neuropathy and cauda equina lesion by lumbar spondylosis. It is noteworthy that elderly individuals commonly have “detrusor hyperactivity with impaired contractile function (DHIC),” which is a combination of detrusor overactivity during bladder filling (due mostly to brain disease, and prostatic hypertrophy in elderly men) and bladder underactivity during voiding as described earlier.68–72 However, the exact pathophysiology of DHIC is still uncertain. In brain diseases, one explanation is that two separate brain areas (the facilitatory and inhibitory brain sites for micturition) might be involved that lead to DHIC. In contrast, in spinal cord lesions, a single partial lesion in the spinal autonomic pathways could cause DHIC, since it disrupts the spino-bulbo-spinal micturition reflex arc, and could cause the emergence of a C-fiber-mediated novel sacral micturition reflex arc below the lesion.54,55 These findings phenotypically mimic motor dysfunction caused by pyramidal tract lesion, i.e., in upper neuron–type spinal cord lesion, muscle weakness inevitably occurs. Concurrently, usually several times later, exaggerated reflexes may become obvious. In the LUT, detrusor-sphincter dyssynergia may further overlap during the voiding phase, which will lead to more severe voiding dysfunction and lower urinary tract symptom (LUTD). Also, concurrent bladder wall damages (age and/or obstruction related) may contribute to these dysfunctions.
Degenerative Diseases of the Nervous System
Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw in Hankey's Clinical Neurology, 2020
Clinical signs outside the spectrum of PD: Oculomotor (e.g. restricted eye movements due to supranuclear gaze palsy).Cerebellar features (nystagmus, dysarthria, wide-based gait, ataxia).Pyramidal tract signs (hyperreflexia, weakness, Babinski's sign).Nondrug-induced myoclonus.Inspiratory stridor.
Biogenic amines
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop in Atlas of Inherited Metabolic Diseases, 2020
Deficiency of TH leads to clinical manifestations very early in life, nearly all by the first-year birthday [24, 25, 28, 29]. The clinical features are such that the diagnosis is mostly not made clinically, but usually by the pattern of metabolites in the CSF (see Table 17.1), so lumbar puncture is an essential step in elucidating the diagnosis. Most patients present with a phenotype that is characterized by a progressive extrapyramidal movement disorder (hypokinetic-rigid syndrome with dystonia) (TH deficiency type A, the recessive DOPA-responsive dystonia). Some can develop normally until an arrest of motor development with a combination of neurologic symptoms before or around one year of age. Hypokinesia, marked truncal hypotonia, mask face, oculogyric crises (see Figure 17.5), myoclonic jerks, and an extrapyramidal tremor develop progressively. The latter three can be mistaken as epileptic phenomena. After infancy, muscle tone increases progressively. Contractures, failure to thrive, and immobilization may develop; (dystonic) cerebral palsy is a likely descriptive (mis-)diagnosis. Some patients who did not develop extrapyramidal symptoms in the first year of life were able to walk independently and followed a clinical course best summarized as spastic paraplegia [27]. Their symptoms resolved completely following L-DOPA supplementation, and they continued to live as healthy and independent adults. Others may have no pyramidal tract or ocular signs but progressive extrapyramidal symptoms mainly dystonia and rigidity [33]. In several patients, TH deficiency has led to infantile-onset parkinsonism [33].
On the origin of the term decussatio pyramidum
Published in Journal of the History of the Neurosciences, 2018
Most fibers of the pyramidal tract of the medulla oblongata cross to the contralateral side and are called the pyramidal decussation (Hirsch, 2000, p. 122). The Latin term decussatio is derived from decussis and means intersection of two lines to form the Roman numeral for 10 (= decem) (Oxford Latin Dictionary, 1968, p. 495). Decussation is a term used in anatomical nomenclature for various other structures as well. Its Greek equivalent is chiasma, derived from Greek character χ (chí). The best-known decussation is the chiasma opticum, but the Latin equivalent decussatio was also used for this in the past. This contribution deals with the history of the term decussatio pyramidum from the point of view of terminology in particular, although of course its technical content cannot be avoided.
Mechanisms of Modulation of Automatic Scapulothoracic Muscle Contraction Timings
Published in Journal of Motor Behavior, 2021
Samuele Contemori, Roberto Panichi, Andrea Biscarini
Our results imply the presence of at least one neural pathway that is capable to modulate the automatic timing of contraction of the scapulothoracic muscles. These muscles receive extensive projections from the extrapyramidal tracts, which are responsible for innate automatic postural/stabilization motor responses (Kandel et al., 2013). The descending cortical projections responsible for the delivering of voluntary motor commands to the spinal motoneurons and interneurons, via the pyramidal tracts, make also connections with the midbrain nuclei from which to the extrapyramidal tracts originate (Noback et al., 2005). Therefore, the midbrain nuclei of the extrapyramidal tracts might represent a candidate hub where the volitional motor commands can modulate the contraction onset time of the scapulothoracic muscles. However, we are mindful that other supraspinal or spinal circuits cannot be ruled out.
Split phenomenon of antagonistic muscle groups in amyotrophic lateral sclerosis: relative preservation of flexor muscles
Published in Neurological Research, 2021
Jingwen Liu, Zhili Wang, Dongchao Shen, Xunzhe Yang, Mingsheng Liu, Liying Cui
We collected clinical information for all patients diagnosed with ALS at their initial visit, including age-at-onset, gender, disease duration, and the region of onset. The patient’s clinical status was assessed using the ALS Functional Rating Scale-Revised (ALSFRS-R) [13]. Muscle strength was monitored by the Medical Research Council (MRC) score including range of motion, with bilateral assessment of the following antagonistic muscle pairs, elbow flexion and extension, wrist flexion and dorsiflexion, finger flexion and extension, knee flexion and extension, ankle plantar flexion and dorsiflexion, and toe plantar flexion and dorsiflexion. The MRC system graded muscle strength as 0, 1, 2-, 2, 2+, 3-, 3, 3+, 4-, 4, 4+, 5-, and 5. To facilitate calculations, we converted the above MRC scale into a modified MRC score corresponding to 1–13 (Table 1). We examined bilateral reflexes in biceps, triceps, radial membrane, knee, and ankle to determine whether the pyramidal tract was involved. Pyramidal tract was thought to be involved in the following cases: (1) Brisk reflexes; (2) The reflexes were not reduced and still be elicited when the muscles were atrophic and weak.
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