1 ite matter dysfunction (i.e., spasticity and hyperreflexia).

2 tion pressure and fewer episodes of detrusor hyperreflexia.

3 ndent depression of the H-reflex, suggesting hyperreflexia.

4 nce rate in neurological exam was 76 for leg hyperreflexia, 53 for leg weakness, and 37 for Babinski

5   We report two patients with delayed-onset, hyperreflexia and gradually progressive disease.

6 ing consequences of post-traumatic autonomic hyperreflexia and post-injury immune suppression.

7 enerative disease characterized primarily by hyperreflexia and progressive spasticity of the lower li

8 ograms because they result in a reduction of hyperreflexia and spasticity.

9 er had progressive weakness, fasciculations, hyperreflexia, and active denervation on electromyograph

10 tuations, benefit from sleep, foot dystonia, hyperreflexia, and early susceptibility to levodopa-indu

11 ensive care unit with coma, hypersalivation, hyperreflexia, and stimulus-induced clonus.

12 2 receptors, offers a partial explanation of hyperreflexia below a chronic SCI.

13 athetic activity and normalizes carotid body hyperreflexia in conscious rats with hypertension; no ef

14  These neurons generate both tonic drive and hyperreflexia in hypertensive (but not normotensive) rat

15 sensation (allodynia) and/or urinary bladder hyperreflexia in the clinical syndrome, interstitial cys

16 t, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, involuntary mus

17 a critical role in the chronic allodynia and hyperreflexia observed after SCI or peripheral nerve dam

18 eborrheic dermatitis, eczema, and persistent hyperreflexia of the lower limbs and with nonsignificant

19 tions ranging from long-term pain to bladder hyperreflexia, we and other groups have sought to develo

20        We hypothesized that the reduction in hyperreflexia with exercise after SCI relies on a return