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At least 19 recordsLinked to original sources
PubMed2005

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes.

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

Contracture↗
PubMed1994

Pure dysarthria, isolated facial paresis, or dysarthria-facial paresis syndrome.

BACKGROUND AND PURPOSE: Pure dysarthria, isolated supranuclear facial paresis, and their combination without somatic motor dysfunction are rarely encountered clinical syndromes and have not yet been clearly characterized. METHODS: Thirteen patients (9 men, 4 women; aged 33 to 72 [mean, 56] years) with unilateral strokes who developed dysarthria with or without facial paresis but without somatic motor dysfunction were reviewed in addition to case reports from previous literature. RESULTS: Computed tomographic scan and/or magnetic resonance imaging showed infarcts on the corona radiata in 4 patients, basal ganglia abutting the internal capsule in 3, basal ganglia-corona radiata in 1, pontine base in 3, and cortical-subcortical bulbar motor area in 2. The dysarthria and facial paresis were usually mild and transient, and either one was likely to be unnoticed. CONCLUSIONS: It is suggested that pure dysarthria or isolated facial paresis syndrome be considered as an extreme continuum of dysarthria-facial paresis syndrome, which is likely to be a variant of dysarthria-clumsy hand syndrome.

Adult↗
PubMed1996

Monocular elevation paresis and contralateral downgaze paresis from unilateral mesodiencephalic infarction.

A 26 year old woman presented with monocular elevation paresis of the right eye, contralateral paresis of downward gaze, and subtle bilateral ptosis. Magnetic resonance imaging disclosed a unilateral embolic infarction restricted to the mesodiencephalic junction involving the left paramedian thalamus. Preserved vertical oculocephalic movements and intact Bell's phenomenon suggested a supranuclear lesion. This rare "crossed vertical gaze paresis" results from a lesion near the oculomotor nucleus affecting ipsilateral downward gaze and contralateral upward gaze fibres, originating in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF).

Adult↗
PubMed2001

Unilateral or localized Reinke's edema (pseudocyst) as a manifestation of vocal fold paresis: the paresis podule.

BACKGROUND: The nosology of free-edge vocal fold lesions remains imprecise. In particular, the lesion termed pseudocyst remains enigmatic, because its histology is poorly defined and because its etiology is unknown. We define pseudocyst as a discrete, unilateral, localized area of Reinke's edema (without a capsule), usually occurring at the midportion of the free-edge striking zone. OBJECTIVE: To report the demographic and clinical findings, as well as discuss our diagnostic and therapeutic strategies, in patients with unilateral Reinke's edema or pseudocyst. METHODOLOGY: All patients diagnosed with unilateral Reinke's edema or pseudocyst over a 2-year period (1998-1999) were identified from the clinical database of the Center for Voice Disorders of Wake Forest University, Winston-Salem, North Carolina. The record of each patient was retrospectively reviewed. RESULTS: Thirteen patients were identified, 12 of whom were female. The mean age was 36 years. Sixty-nine percent (9 of 13) had unilateral pseudocyst and 31% (4 of 13) had unilateral Reinke's edema. All patients had documented vocal fold paresis on laryngeal electromyography. The 9 patients with pseudocyst underwent excision of their lesions; 7 had bilateral medialization laryngoplasties, 1 had lipoinjection, and 3 did not have surgical intervention. Significant improvement was noted postoperatively on a self-administered glottal insufficiency (symptom) index (P <.001). CONCLUSION: Unilateral Reinke's edema and localized Reinke's edema (pseudocyst) are distinct clinical entities, occurring most frequently in women in their fourth decade. The finding of unilateral Reinke's edema or pseudocyst should alert the clinician to the likelihood of vocal cord paresis. Surgical intervention with medialization laryngoplasty appears to be beneficial.

Adult↗
PubMed2004

[Not all vocal cord failure following thyroid surgery is recurrent paresis due to damage during operation. Statement of the German Interdisciplinary Study Group on Intraoperative Neuromonitoring of Thyroid Surgery concerning recurring paresis due to intubation].

Since the phoniatrician H. Bauer described the first case of recurrent laryngeal nerve palsy most likely caused by intubation some 45 years ago, several case reports have been published. However, systematic analyses regarding the frequency of recurrent laryngeal nerve palsies due to intubation are scarce, and none of them has used the proper methods to demonstrate clearly that such a mechanism exists. Currently available data justify the assumption that not every recurrent laryngeal nerve palsy following thyroid surgery is due to the operation itself and that the damage caused by intubation, however, may only account for a minority of these cases. The differential diagnosis of postoperative recurrent laryngeal nerve palsy requires the use of specific tools which go beyond simple laryngoscopy and include stroboscopy as well as intra- and extralaryngeal electromyography. A partial palsy of recurrent laryngeal nerve due to intubation would be associated with severe dysphonia or aphonia, not with dyspnea because of the typical intermediate position of the paralyzed vocal folds with a normal electromyographic function of the cricothyroid muscle. The use of these methods to identify the nature of postoperative recurrent laryngeal nerve palsy is recommended in cases of regular intraoperative neuromonitoring but postoperatively impaired function of the vocal cords.

Diagnosis, Differential↗
PubMed2001

[Bilateral ptosis, bilateral upgaze and adduction paresis, and monocular downgaze paresis from a mesencephalic infarction].

We report a 57-year-old man with an ischemic lesion in the midbrain. In the acute stage, he presented with bilateral ptosis and markedly limited extraocular motion except for bilateral abduction and downward motion of the right eye. The pupillary reaction to light of his left eye also was impaired. He was admitted to our hospital, and brain MRI showed a small infarction extending from the left paramedian to the median tegmentum of the midbrain. Three weeks after admission, the ptosis and limited extraocular right eye motion had resolved. The pupillary reaction and downward motion of the left eye normalized gradually within 3 weeks. Two months after admission, ptosis and the limited left eye adduction were partially resolved, but the markedly limited upgaze of the left eye had not changed. Initial neuro-ophthalmologic findings suggested involvement of the caudal part of the oculomotor nucleus and the left oculomotor nerve within the midbrain. The pattern of neuro-ophthalmologic impairment seen in our patient led us to conclude that the caudal oculomotor nucleus and medial part of the fascicular fibers of the left oculomotor nerve probably recovered first, after which recovery of the fascicular fibers progressed laterally. The results of serial MRI were consistent with this interpretation.

Abducens Nerve Diseases↗
PubMed1977

[An index for paresis and defective healing--an easily applied method for objectively determining therapeutic results in facial paresis (author's transl)].

Residuals of facial paralysis consist of a great variety of cosmetic and functional anomalies which differ in quality and/or quantity. An internationally standardized evaluation of such defects is mandatory for the assessment of the results of different therapeutic procedures. In the present study, a system has been developed to record the results of facial paralysis following therapy. Such a system does not require specialized training, instrumentation or require significant time for completion. A clearly-defined "Yes-No" evaluation criteria is established which creates a high interscorer reliability. The usefulness of this scoring system was tested by three examiners on 42 patients following facial nerve surgery, with an obtained interscorer reliability of 93%.

Eyelid Diseases↗
PubMed1998

Recovery of arm function in patients with paresis after traumatic brain injury.

OBJECTIVE: To characterize the frequency of recovery of arm paresis in patients with traumatic brain injury (TBI) admitted to rehabilitation. DESIGN: Retrospective review identifying a cohort of patients with moderate or severe arm paresis after TBI followed at least 6 months postinjury. SETTING: Freestanding acute rehabilitation hospital TBI unit. PATIENTS AND METHODS: Forty-four patients with moderate to severe arm paresis were selected from 264 consecutive admissions and characterized by injury pathology subtype, injury severity (duration of unconsciousness [loss of consciousness, LOC] and posttraumatic amnesia [PTA]), age, and level of paresis according to Brunnstrom Stages of Recovery (BS 1 to 6). Patient groups with and without arm paresis were compared according to these variables (t tests and chi(2)). MAIN OUTCOME MEASURES: Recovery of arm paresis to isolated motor function (BS 5 or 6) and time to achieve recovery. Recovered and nonrecovered patients were compared (Mann-Whitney, t tests, and chi(2)) on injury severity, initial level of paresis, age, time to rehabilitation admission, and pathology subtype. Time to recovery was compared for patients at different levels of initial paresis, ranges of LOC, and pathology subtypes (Mann-Whitney and Kruskal-Wallis tests). RESULTS: Forty-four patients (17%) had moderate (BS 3 to 4) or severe (BS 1 to 2) paresis at rehabilitation admission. They were more severely injured than nonparetic patients based on longer LOC (p < .002) and PTA (p < .009). Thirty-six patients (82%) recovered by 6 months; 72% of these recovered by 2 months. If still paretic at 2 months, only 56% recovered. Mean recovery time was 6.9 weeks (SD, 6.1) from injury. Time to recovery was best predicted by initial level of paresis and injury severity (r2 = .48), but not age. Patients with diffuse injury tended towards a more protracted recovery (7.9 weeks, SD 6.5) than patients with focal injury (4.2 weeks, SD 3.9) (p = .08) and only those with diffuse injury showed further recovery after 3 months. CONCLUSIONS: Arm paresis after TBI is relatively infrequent. Most patients recover by 2 months but later recovery is possible, especially in patients with primarily diffuse brain damage. Recovery is highly related to initial impairment, injury severity, and distribution of brain injury.

Adolescent↗