Practice Pearls in Neurology—Series II AV Srinivasan, D Vasudevan, Bhanu Kesavamurthy
INDEX
Page numbers followed by b refer to box, f refer to figure, fc refer to flowchart, and t refer to table.
A
Acetaminophen 88
Acetylcholine 7
Acquired epileptic aphasia 23
Actinomyces israelii 36
Actinomycosis 36
Adrenergic antagonists 8
Agnosia training 69
Alexia 70
Alfuzosin 8
Alveolaris 42
Alzheimer's disease 58
Amantadine 95
Amikacin 41
Amino acids 49
Amphotericin
B 41
deoxycholate 46
lipid complex 44, 46
lipid formulation of 46
Amyloidosis 13
Ankle-foot orthosis 117
Anterolisthesis, grade 2 83f
Antibiotic 34, 41
therapy, long-term 39
Anticholinergics 95
Antidromic sensory recording 14
Antiepileptic medications 28
role of 28
Antifungal therapy 49
Anti-inflammatory effects 124
Antimuscarinic drugs 7, 7t
Antineutophilic cytoplasmic antibody 51
associated diseases 51
Antiparkinsonian medications 74
Anti-siphon devices 63
Anxiety 28
Apathy 95
Apophysomyces 45
Apparent disc herniation 83f
Apraxia
interventions for functional limitations to 69
training 68
Arachnoid cyst 83f
Artery thrombosis, median 13
Aspergillosis 48
Aspergillus fumigatus 48
Astereognosis 70
Astrocytoma 82f
Atherosclerotic plaques 124
Atorvastatin 124, 125
Atrial fibrillation 108
Attention deficits 67, 68
Audiovestibular damage 50
Auricular chondritis, bilateral 50
Autoimmune thyroid disease 112
Autoimmune thyroiditis 112
Automatic brain systems 67
Autonomic nervous system 74
Azathioprine 50, 51
Azithromycin 39, 41
Azoles
like fluconazole 41
like voriconazole 49
B
Babinski sign 91
Back pain, without 85fc
Baclofen 8
Bacterial infections 33
Balamuthia mandrillaris 41
Bartonella henselae 39
Basedow's paraparesis 109
Behavioral techniques 5
Behçet's disease 51
Benzodiazepines 8
Birbeck granules 54
Bladder
dysfunction 2f
expression 6
innervation, anatomy of 1, 1f
neck dyssynergia 3
reflex, cortical regulation of 3
sphincter procedure 9
Blake's pouch cyst 58
Blood
pressure 105t
increasing 95
Blood-brain barrier 124
stabilization of 124
Body bradykinesia 104
Botulinum toxin 9
Brachial plexopathy 13, 16
Bradykinesia 73, 75, 91, 98
Bragard's sign 85
Brain
stimulation techniques 70
tumor cortical trauma 3
Broca's area 70
Brucellosis 34
Buddha's hand appearance 40, 40f
C
Candidiasis 47
Carbimazole 109
Cardiopulmonary impairment 97
Carpal tunnel 12
cross sectional anatomy of 12f
lipoma 13
surface anatomy of 12f
surgical decompression of 18f
syndrome 12, 13, 13b, 14t, 16, 16b, 17, 111
grading severity of 14t
Caspofungin 49
Cat scratch disease 39
Cauda equina syndrome 1, 81f
Ceftriaxone 34
Cell proliferation, regulation of 127
Central disc herniation 81f
Central nervous system 31, 33, 34, 36, 37, 47, 48, 51
toxoplasmosis 42
Centro temporal
electrodes 24f
spikes 23, 24f
Cerebellar atrophy 54
Cerebral
abscesses 37, 47
artery, middle 35, 42
paragonimasis 40
recovery after stroke 65fc
schistosomiasis 40
syphilitic gumma 36
Cerebrospinal fluid 34, 39, 41, 42f, 44, 57
block, complete 87f
flow 61
outflow studies 62
Cerebrovascular accidents 108
Cerebrovascular diseases, current role of statins in 123
Cervical radiculopathy 13
Childhood epilepsy, benign 23
Chlorambucil 51
Cholesterol
levels, aggressive reduction of 125
synthesis 127
enzyme in 123
inhibition of 123
Cholestyramine 110
Cholinergic agonists 8
Chorea 108
Choroid plexus 53
Chronic disability, cause of 65
Churg-Strauss syndrome 51
Cingulate sulcus
posterior half of 60f
sign 60f
Clonazepam 77
Clonidine 8
Closed-fist sign 14
Coccidioidal meningitis 47
Coccidioides immitis 46, 47
Coccidioidomycosis 46
Cognitive impairment 65, 107, 111
Cognitive training 67
Collagen disease 13
Comorbid psychiatric illness 28
Compound muscle action potential 14, 16
Computed tomography 59
scan 41
Condom catheters 5, 7
Conduction velocity 15
Confusion arousals 73, 77
Congenital thenar hypoplasia 13
Consolidation therapy 45
Cortical micturition center 1
Cortical venous thrombosis 108
Cotrimoxazole 41
Cranial nerve
involvement 38
palsy 34, 49
Creatine kinase 109
Cryptococcal disease 44
Cryptococcosis 44
Cryptococcus neoformans 44
Cunninghamella 45
Cutting food and handling utensils 102
Cyclophosphamide 50, 51
Cyclosporin A 50
Cystometrogram 4
Cystoscopy 4
D
Daily living, activities of 68
Dapsone 50
Darifenacin 7
Deep brain stimulation 30, 97
chronic 97
Dementia 5, 57, 94, 101, 111
Dental care 96
Denture retention 96
Depression 95, 101
Detrusor
areflexia 3
external sphincter dyssynergia 3
hyper-reflexia 3
hypoactivity 6
sphincter dyssynergia 2
Diabetes mellitus 3, 13
Diazepam 8
Dibenzyline 8
Diffusion tensor imaging 86
Digiti minimi, abductor 19
Disc
degeneration 81
herniation
multiple 79f
posterolateral 81f, 82
material, superior migration of 83f
migration 79f
prolapse 81
with inferior migration, extruded l3-l4 81f
Discitis 80
Distal median motor latency 14
Domain-specific training 66
Dopamine 119
agonists 77
Doxepin 77
Doxycycline 33, 34, 39
Dressing 102
Dysautonomic symptoms 73
Dyschondroplasia 13
Dyskinesia 75, 104
drug-induced 98
painful 105
reappear 76
Dystonia
painful 75
presence of early morning 105
E
Echinococcosis 42
Echinococcus granulosus 42
Electroencephalography 23, 27f, 70, 108
Electromyogram 26
Electromyography 4, 15, 19, 19t, 21t, 27f
Electro-oculogram 27
Electrophysiological tests 14
Embolic strokes 126
Encephalitis 33, 34
Endoscopic third ventriculostomy 62
Endothelial nitric oxide synthase 123
Enterocystoplasty 9
Enzyme-linked immunosorbent assay 33
Eosinophilic granulomatosis 51
Epididymitis 7
Epididymorchitis 7
Epidural abscess 80
Epilepsy 22, 26, 28, 31
syndromes 23
genetic generalized 23
Epileptic encephalopathy 23
Epileptic seizures 27
Errorless learning 67
Eszopiclone 77
Evans’ index 60
Excessive daytime sleepiness 26, 28, 73
Exploration training 69
Eye signs 113t
F
Facial expression 103
Fajersztajn's crossed sciatic sign 85
Fatigue 33, 71
Fibroblasts transplantation 10
Fibrous histiocytoma, benign 54
Fixed differential pressure valves 62, 63
Flexor carpi
radialis 12, 19, 21
ulnaris 12
Flexor digitorum
profundus 12
superficialis 12
Flexor pollicis longus 12
Flick sign 14
Flow-regulated valve 62, 63
Fluconazole 47
Flucytosine 41
Focal epilepsy syndromes 23
Frisch bacillus 38
Fungal infections 44
G
Gait 98, 104
apraxia 58
disturbance 5759, 94, 100
Gamma-aminobutyric acid 8
Ganglion 13
Gastrointestinal problems 96
Globus pallidus 98
Glutamate 49
Glutamine 49
Glutathione peroxidase 124
Goiter 107
Gout 13
Granulomas 32
Granulomatosis 51
Granulomatous
amebic encephalitis 41
disease, idiopathic non-caseating 52
Gravity-assisted valve 62, 63
Great auricular nerve 38
H
Hakim's triad 57
Hallucinations 73, 95
Hashimotos encephalopathy 112
Headache 33, 34
Hematuria 7
Hemorrhagic stroke 127
Hepatic cholesterol synthesis 123
Herpes zoster 3, 13
High intensity 126
statin therapy 126
Hip joint 85
Hodgkin's disease 13
Human immunodeficiency virus 36
Hydatid cyst, treatment of 42
Hydrocephalus, idiopathic normal pressure 5759
Hygiene 102
Hyperadrenergic state 108
Hyperinsulinemia 108
Hypersensitivity 32
Hypersomnia 75
Hyperthyroidism 107
management of 109
neurological manifestations of 107
Hypnogram 29
Hypoglycemia 110
Hypokinesia 104
Hyponatremia 110
Hypotension 110
Hypothalamic-pituitary axis 53
Hypothenar muscles
wasting of 13
weakness of 13
Hypothyroid myopathy 111
Hypothyroidism 107, 110, 111
fetal 110
management of 111
neonatal 110
neurological manifestations of 110
Hypoventilation 110
I
Inching technique 15
Infectious diseases 32
Inflammatory demyelinating polyneuropathy
acute 113
chronic 113
Insane, general paresis of 35
Insomnia 75
treatment of 76
Instability pain 82
Intensity
low 126
moderate 126
Interlaminar epidural steroid 89
Intermittent catheterization 9
Intervertebral disc 81f
Intoxication, drug 101
Intracranial intra-axial lesions 54
Intracranial pressure 61, 62
Intramedullary tumor 82f
Intraparenchymal lesions 54
Intravenous methylprednisolone 51
Isavuconazole 46, 49
Ischemic stroke 119, 125
Isoprenoid 123
synthesis, inhibition of 123
Itraconazole 41, 45
J
Juvenile myoclonic epilepsy 23
K
Kidney ureters bladder 5
Klebsiella rhinoscleromatis 38
Kocher-Debre-Semelaigne syndrome 111
Kyphoscoliosis 87f
L
Landau-Kleffner syndrome 23
Langerhans cell histiocytosis 53, 54
diagnosis of 54
Lasegue's sign test 85
Leflunomide 52
Leprosy 37
multibacillary 38
Leucocyte oxidase defect 32
Leukemia 13
Levodopa 74, 97, 111
induced dyskinesias 76
Levofloxacin 39
Levothyroxine, doses of 111
Lighthouse strategy 66
Limbic encephalitis 49
Liothyronine 110
Lipid-lowering drug 123
Lipoprotein
low-density 123
non-high-density 127
Liposomal amphotericin 48
Lobe epilepsy
and parasomnia scale, frontal 25
nocturnal
frontal 23
temporal 23
Low back ache 79
chronic 88
clinical examination 84
electrophysiological studies 88
epidemiology 79
evaluation of 79, 80
interventional therapy 89
magnetic resonance imaging 86
management of 79, 86, 88
myelography 87
neurological examination 85
pharmacological management 88
psychological screening 86
radiation therapy 89
Low back pain 79, 80fc
assessment of 87
Lumbar canal stenosis 82
severe 79f
Lumbar lordosis, exaggeration of 79f
Lumbo-peritoneal shunt 62
Lyme disease 33
M
Magnetic resonance imaging 16, 25, 33, 34, 36, 37, 40, 41f, 42, 45, 51, 52, 59, 70
flair 42f
functional 70
Matrix metalloproteinases 124
McAdam's diagnostic criteria 49
Melkerson-Rosenthal syndrome 38
Memory
functional 67
notebook 67
training strategies 68fc
Meningitis 34
acute 35
basal 34
chronic 34
Meningoencephalitis 34
Meningovascular syphilis 35, 36
Metabolic disorders 84
Metacognitive strategy training 67
Methimazole 109
Methotrexate 50, 51
Micafungin 49
Mickulicz cells 39
Micturition, supraspinal regulation of 1
Minocycline 38
Mobility 120
Mononeuritis multiplex 13
Mononuclear predominant inflammatory cells 32
Mood disorders 71
Motor abnormalities 94
Motor disability, interventions and 117
Motor dysfunction, contribution of 75
Motor examination 103
Motor fibers 3
Motor fluctuations 94
Motor neuron disease 13
Motor problems 94
Motor recovery from stroke, pharmacological medications in 118
Movement disorders 108, 111
Mucormycosis 45, 46f
Multimodal neuroenhancement, effect of 70
Myasthenia gravis 112
Mycobacterium leprae 37
Myelitis 34, 39
Myeloma, multiple 13
Myelomeningocele 3
Myelopathy 13, 34, 40
Myopathy 109
Myxedema coma 110
N
Nasal chondritis 50
Neck pain 13
Needle electromyography 15
Neonatal hypothyroidism 110
Neoplastic granulomas 53
Nerve
compression of 12
conduction study 18, 18f, 19, 20t
median 14
paralysis, quiet 37
Neurobehavioral impairments 66
Neuro-Behçet's disease 50
Neurobrucellosis 34
Neurocognitive dysfunction, treating 71
Neurodegenerative disease 54, 91
Neurodevelopmental therapy 116
Neuroenhancement tools 66, 70
Neurofeedback 70
Neurofibromatosis 13
Neurogenic bladder 1, 4t, 5, 7, 8, 8t, 9
dysfunction 3, 5fc
Lapides classification of 3, 3t
management of 1
Neurogenic detrusor overactivity 3, 7
Neurogenic intrinsic sphincter deficiency 3
Neurogenic lower urinary tract dysfunction 1
Neurologic disorders 3b, 10
Neurological deficit 85fc
Neurological disease
signs of 34
symptoms of 34
Neuromodulation 9
Neuromuscular electrical stimulation 118
Neuropathy, silent 37
Neurorehabilitation, neuroenhancement methods of 70b
Neurorehabilitative methods 71
Neuroretinits 39
Neurosarcoidosis 52
Neurosyphilis 35
asymptomatic 35
Nicotinamide adenine dinucleotide phosphate 123
Nightmares 73
Nitric oxide synthesis, modulation of 124
Nocturia 74
Nocturnal paresthesias 13
Nocturnal-akinesia 77
Nodular enhancing lesions, multiple 40f
Nonergot dopamine agonist 75
Noninvasive brain stimulation techniques 118
Nonminor strokes 126
Nonmotor problems 94
Nonpharmacologic therapy 98
Nonpharmacological treatment 88
Nonrapid eye movement 22, 73
Nontuberculous granulomas 54
Nuclear scans 88
Nutritional disturbances 97
O
Obstructive sleep apnea 26, 29
Occipital paroxysm 23
Occupational therapy 100
Ocular inflammation 50
Oflaxacin 38
Olfactory ensheathing cells 10
Optic atrophy 35
Orthostatic hypertension 95
Osteomyelitis 80
Osteophyte formation 83f
Oxybutynin 7, 8, 77
P
Pacemaker 87
Pachymeningitis 49
Pad test 4
Pain 13, 18
etiology, evaluation of 80
localized acute 83
localized spinal 80
Panayiotopoulos syndrome 23
Panic attacks 73
Paracentral lobule 1
Parasitic infections 39
Parasomnia 75
Paraspinal region 84
Paresthesias 13, 33
Parkin-gene 92
Parkinson's disease 59, 73, 75, 91, 98
adaptation of 98
advanced 94, 96
assessment scales in 101
diagnostic criteria for 92
disability in 100
environmental modifications 98
epidemiology 92
etiological factors 92
management of 91
pharmacological management 94
polysomnography in 76
psychotherapy and counseling 100
sleep
disorders in 73
disturbance in 75
surgical management of 97
unified 101t
Parkinson's patients 94, 96
Paroxysmal attacks 23, 26
Paucibacillary leprosy 38
Pelvic
floor muscle 6
plexus lesions 1
trauma 3
Penile clamp 5
Pentamidine 41
Perceptual and cognitive impairment 66
Perceptual deficit, interventions for 66, 67b
Perceptual performance 66
Periodic limb movement 73
disorder 26
in sleep 76
Peripheral nervous system 33, 51
Peripheral neuropathy 13, 109
Pernicious anemia 3
Peroneal nerve 38
superficial 38
Persistent axial stiffness, severe 82
Phalen's maneuver 13, 18, 20
Phalen's test 13, 14
Pharmacologic treatment 74
Pituitary bright spot, posterior 53f
Plantar fasciitis 13
Plaque, stabilization of 124
Plasmapheresis 52
Pollicis brevis, abductor 19, 21
Polyangiitis 51
Polychondritis, relapsing 49
Polycythaemia 13
Polyenes 49
Polyneuropathy 16, 111
coexistent 16
Polysomnography 26, 29
Pontine micturition centre 1
Posaconazole 49
Positive airway pressure, continuous 30, 77
Post-Lyme disease syndrome 33
Poststroke
aphasia 70
depression 119
Postural tremor of hands, action of 103
Posture 104
and alignment changes 85
Postvoid residual bladder volume 4
Pramipexole 75
Praziquantel 40, 41
Pressure hydrocephalus
classification of normal 58fc
normal 57, 58, 60f
secondary normal 58
Pressure provocation test 14
Pretibial myxedema 107
Prolapsed disc material 81f
Pronator teres 19, 21
Propamidine isethionate 41
Propylthiouracil 109
Prosopagnosia 69
Prostatitis 7
Proximal median
lesion 15
neuropathy 13
Psychogenic nonepileptic attack disorder 26, 27
Psychosis 95
affects 74
Pudendal nerve 1
Pulse 105t
Pure word deafness 70
Purulent lesions, chronic 48
Pyogenic granuloma 54
Pyrimethamine 43
Q
Quality of life 22
R
Radial nerves, superficial 38
Radial neuropathy 13
Radiculopathy 40
Radio iodine ablation 110
Ramelteon 77
Randomized clinical trials 8
Rapid eye movement 22, 73
parasomnia 26
sleep, normal 27f
Raynaud's phenomenon 13
Reactive oxygen species 124
Reflex 3
Rehabilitation 98
Renal failure 13
Renal function studies 4
Respiratory
muscle dysfunction 74
tract chondritis 50
Restless legs syndrome 29, 73, 76, 95
Retropulsion of fragments, L1 fracture with 84f
Rheumatoid arthritis 20
Rhinoscleroma 38
Rhizomucor 45
Rifampicin 34, 39
Rifampin 41
Rigidity, role of 75
Ring enhancing lesions, multiple 43f
Rituximab 52
Rolandic epilepsy 23
benign 24f
S
Sacral nerve rerouting 10
Sacral spinal cord lesions 1, 2
Sacroiliac joint tenderness 85
Sarcoidosis 13, 52
Schistosoma
haemotobium 39
japonicum 39, 40
mansoni 39
Schistosomiasis 39
Schwann cells 10
Sclerosis, multiple 13, 33
Seborrheic dermatitis 97
cause of 97
Seizures 3, 34, 49, 108
Sensory
deficit, interventions for 66
disturbance 13
fibers 3
nerve 14
action potential 16, 17
tests, computerized quantitative 38
Sensory-evoked potentials 88
Serotonin reuptake inhibitors 116, 119
Shunt systems, types of 62
Sialorrhea 96
Sicard's sign 85
Single-photon emission computed tomography 36
Sleep 22
apnea 74
behavioral disorder 73
disorders 22, 30, 73, 95
primary 28
treatment of 29
disturbance 73
symptoms of 75
electroencephalography 30
fragmentation 95
latency test, multiple 29
maintenance insomnia 75
problems 77
regulating structures, primary involvement of 73
related breathing disorders 77
terrors 23
Sleepwalking 23
Slow-wave sleep 26
Snoring 73
Soap bubble appearance 41
Solifenacin 7
Speech 98
and language 70
rehabilitation 71b
therapist 96
therapy 100
Sphincterotomy 9
Spinal cord 3, 33
injury 3, 5
lesions 10
suprasacral 1, 2
regeneration 10
tumors 82
Spinal fibers 3
Spinal tap, routine 61
Spine
imaging of 86
problems, degenerative 82
Splinting 17f
Spondylolisthesis 79f, 83f
Spondylolysis 82
Spondylotic, extensive 83f
Square wrist 14
Static cystogram 4
Steroid 50, 110
responsive encephalopathy 112
Stopping maintenance therapy 45
Straight leg raising test 85
Strategy training 68
Streptomycin 34
Stroke 3, 49, 65, 120
and motor recovery 116
cerebral recovery after 65
left hemispheric 70
management of 125
part of 123
nonmotor rehabilitation in 65
patients
fitness in 120
rehabilitation in 116
prevention 125
recovery phase after 116
severity 120
Stroke-related disability 71
Subdural hygroma 63
Sulfadiazine 43
Sulfamethoxazole 34, 43
Superoxide dismutase 124
Supraclavicular nerve 38
Suprapontine lesions 1
Suprapubic catheters 5
Suprapubic cystostomy 7
Supratentorial atrophy 54
Sural nerves 38
Swallowing problems 96
Sylvian fissure 60
Symptomatic orthostasis 105
Syphilis, advanced 3
Syphilitic meningitis, acute 35
Syringomyelia 13
T
Tabes dorsalis 35
Tactile agnosia 70
Temporal lobe epilepsy, bitemporal 23f
Tenderness and muscle spasm 84
Terazosin 8
Terminal latency index 15
Tetrahydrobiopterin 124
Thalidomide 51
Thenar eminence
wasting of 13
weakness of 13
Therapeutic traditional physical approach 116
Thionamides, class of 109
Thoracic outlet syndrome 13
Thought disorder 101
Thyroid
associated eye sign 113
associated orbitopathy sign 113, 113t
bruit 107
disease 107
neurological manifestations of 113
disorders, neurological manifestations of 107
dysfunction 107
hormone 107
imbalance, neurological manifestations to 107
replacement 111
ophthalmopathy, management of 110
stimulating hormone 111
Thyrotoxicosis 107
Thyrotropin-releasing hormone 111
Tibial nerves, posterior 38
Tinel's sign 13, 14
over median nerve 13
Tingling sensations 18
Tizanidine 8
Tolterodine 7
tartrate 8
Tonic clonic seizure 25f
generalized 23
Topographic disorientation 69
Transcranial direct current stimulation 70, 118
Transcutaneous electrical nerve stimulation 6
Transient ischemic attacks 126
Transurethral catheters 5
Transverse myelitis 3, 5, 33
Trauma 83
Trazodone 77
Treating stroke patients 116
Tremor 98, 102
role of 75
Treponema pallidum 35
Triceps reflexes 13
Tricyclic antidepressant 7
drugs 8
Triggered reflex voiding 6
Trimethoprim 34
Trospium 77
chloride 7, 8
Tuberculosis 13
Tunnel signs 41
Tunnel syndrome 13
U
Ulnar abnormalities 16
Ulnar interossei distal motor latency 15
Ulnar nerve 38
dorsal cutaneous nerve of 38
Ulnar neuropathy 13
Ultrasonography 15
Umbilical hernia 110
Upper motor neurons 8
Urethral false passages 7
Urethral trauma 7
Urethritis 7
Urinary
incontinence 57, 58
tract
infection 7, 9
symptoms, lower 4
V
Vacuum phenomenon 83f
compression fracture with 84f
Vagal nerve stimulation 30
role of 30
Vanilloids 8
Vasculitides 113
Vasculitis 32, 34
Vasculopathy 113
Ventriculoatrial shunt 62
Ventriculoperitoneal shunt 62
Vesicoureteral reflux 9
Visual
agnosia 69
neglect 66
restitution training 67
Visuospatial deficit, interventions for 66, 67b
Vivid dreams 73
Voriconazole 41
W
Wegner's granulomatosis 51
Wernicke's area 70
Worm-Eaten sign 41
Z
Zolpidem 77
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Chapter Notes

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Management of Neurogenic BladderCHAPTER 1

M Thangaraj,
Jithin A Bose
 
INTRODUCTION
Neurogenic bladder (NB) or neurogenic lower urinary tract dysfunction (NLUTD), a dysfunction of the urinary bladder and urethra due to disease of the central or peripheral nervous system. Various neurological diseases like stroke, dementias, Parkinson's disease, spinal injuries, spinal tumors, congenital lesions like spinal dysraphism and diabetes can produce NB/NLUTD. The neurogenic dysfunction manifest as over active or underactive bladder which depends on extent and level of neural lesion. It is not only a medical problem but also a major social issue.1
 
ANATOMY OF BLADDER INNERVATION (FIG. 1)
Autonomic Innervation:
  • Parasympathetic: S2- S4 motor to detrusor, inhibitory to internal sphincter
  • Sympathetic: D10-L2 motor to sphincter, inhibitory to detrusor
  • Origin: Intermediolateral grey column.
Somatic:
  • Pudendal nerve (S2, S3, S4)
  • Origin: Nucleus of Onuf/Ventral horn.
Cortical Micturition Center:
  • Second frontal gyrus (Paracentral lobule) inhibitory to PMC.
Pontine Micturition Centre:
  • Supraspinal regulation of micturition.
zoom view
FIG. 1: Anatomy of bladder innervation.
Briefly, neurologic voiding dysfunctions can be classified as (Fig. 2):
  • Suprapontine lesions
  • Suprasacral spinal cord lesions
  • Sacral spinal cord lesions
  • Cauda equina and pelvic plexus lesions.2
zoom view
FIG. 2: Bladder dysfunction due to lesions at various levels.
The suprapontine areas are responsible for providing inhibitory signals to the pontine micturition center, which provides signals for regulating micturition. Suprapontine lesions such as dementias, CVAs, and brain tumors can therefore cause loss in inhibitory signals to the pontine center, resulting in urinary frequency, urgency, urge incontinence, and uninhibited voiding. But there is no impact on the coordination of the bladder and sphincter.
Suprasacral spinal cord lesions result in the loss of supraspinal input. This loss of input typically results in uncontrolled activation of the micturition reflex, via afferent fiber stimulation, causing uninhibited detrusor contractions. Signals from the pons that help to coordinate bladder and sphincter activity can be affected, resulting in detrusor-sphincter dyssynergia (DSD). Detrusor-sphincter dyssynergia occurs more frequently with higher spinal lesions.
Sacral spinal cord lesions can manifest with varying degrees of upper and lower motor neuron damage. This can result in different clinical manifestations, including detrusor hyper-reflexia and areflexia. Similarly, the external sphincter can be affected in different ways, ranging from complete loss of function to DSD.
Lesions that are distal to the sacral spinal cord, such as those present in myelodysplasia, cauda equina injury, radical pelvic surgery, or pelvic plexus injury can result in an areflexic, hypotonic, or flaccid bladder and a denervated sphincter. The external sphincter can be in a 3fixed position, resulting in chronic obstruction and consequent loss of bladder compliance.
 
Functional Classification of Neurogenic Bladder Dysfunction (Box 1)
The functional system is perhaps the most simple and widely accepted classification system for lower urinary tract disorders. First proposed by F. Brantley Scott's group in 1968,2 this system was later popularized by Alan J. Wein.3 In its essence, this system describes whether the deficit is primarily one of:
  • The filling/storage or
  • The emptying/voiding phases of micturition.
A failure of filling/storage and failure of emptying/voiding can result from either bladder or outlet abnormalities, or a combination of both.
 
Lapides Classification of Neurogenic Bladder4 (Table 1)
This classification is useful and easy for understanding and remembering. But some patient may not fit into any one category.
 
EVALUATION (TABLE 2)
As always the patient history is an essential part of the diagnosis. Duration and level of lesion and previous medical histories are important data. The special history includes a complete review on the general neurological, specific somatic and sensory, urinary, anorectal, sexual, gynecological symptoms and signs. Sensations of bladder filling have to be asked for. Autonomic dysreflexia has to be investigated if a spinal lesion above T6 has occurred. The way bladder emptying has been done so far, the eventual presence of incontinence, and any usage of catheter or appliances are important. Evaluation following soinal cord injury is summarized in flow chart 1.
Table 1   Lapides classification of neurogenic bladder
Type
Pathogenesis
Possible etiology
Symptoms
Sensory
Damage to sensory fibers from bladder to spinal cord
Diabetes mellitus, pernicious anemia, advanced syphilis
No bladder sensation. Eventual loss of motor function
Motor
Damage to motor fibers from spinal cord to bladder
Herpes zoster, pelvic trauma, surgery
Normal sensation. Failure of motor function
Autonomous
Damage to both motor and spinal fibers between bladder and spinal cord
Pelvic trauma, low myelomeningocele, surgery
Failure to generate bladder contraction, loss of bladder sensation
Uninhibited
Injury to cortical regulation of bladder reflex
Stroke, brain tumor cortical trauma
Normal sensation and motor function urge incontinence, urinary frequency
Reflex
Damage to spinal cord between sacrum and brainstem
Spinal cord injury, myelomeningocele, transverse myelitis
Poorly coordinated bladder function, loss of sensation, incontinence
4
Table 2   Important investigations in patients with neurogenic bladder
Tests
Uses
Urinalysis with cytology and culture
  • Helps to find urinary tract infection,
  • Hematuria, urinary casts etc. and will help in planning additional investigations like cystoscopy
Renal function studies
Blood urea nitrogen and creatinine helps to assess renal function and renal failure
Voiding diary
Records the patient's bladder activity. It gives information about voiding pattern, incontinent episodes, and provocative events
The pad test
Objective test that documents and quantifies urine loss and the severity of incontinence
Postvoid residual bladder volume (PVR)
PVR tells about under active detrusor or outlet obstruction. Both of these conditions produces urinary retention with overflow incontinence
Uroflow rate
  • Uroflow is a simple non-invasive urodynamic measurement. It measures the volume/time of urine accumulation. Combined with PVR, it is an excellent screening test for bladder outlet obstruction and LUTS (Lower Urinary tract symptoms)
  • Low uroflow rate indicates urethral obstruction, weak detrusor, or combination of both
Filling cystometrogram (CMG)
Provides information on bladder storage capacity, sensation, compliance of bladder (ability to expand during increasing volume of urine), presence or absence of detrusor over activity
Voiding CMG
Records the voiding detrusor pressure and the rate of urinary flow. Only test available to assess bladder contractility and the severity of a bladder outlet obstruction can be combined with video urodynamic study and voiding cystogram in complicated cases of incontinence
Static cystogram
Helps to confirm the presence of stress incontinence, the degree of urethral motion, cystocele and vesico-vaginal fistula or bladder diverticulum
Electromyography (EMG)
EMG allows accurate diagnosis of the detrusor sphincter dyssynergia that is common in spinal cord injuries
Cystoscopy
  • Allows discovery of bladder lesions (e.g., bladder cancer, bladder stone) that would remain undiagnosed by urodynamics alone.
  • Indicated in persistent irritative voiding symptoms or hematuria
Video urodynamics
  • Video urodynamics is the criterion standard for evaluation of a patient with incontinence. Video urodynamics combines the radiographic findings of voiding cystourethrogram and multichannel urodynamics
  • Video urodynamics enables documentation of lower urinary tract anatomy, such as vesicoureteral reflux and bladder diverticulum, as well as the functional pressure-flow relationship between the bladder and the urethra
 
MANAGEMENT
The main objectives for current strategies in the management of NB are:
  • Protection of the upper urinary tract
  • Restoration of the lower urinary tract function
  • Improvement of urinary continence
  • Improvement of the patient's quality of life (QoL).5
zoom view
FLOWCHART 1: Diagnosis and follow-up of patients with neurogenic bladder dysfunction.
 
Conservative Treatment
Most widely applied treatment modality in NB. Conservative treatment is cheap, easily available even in periphery where urologists not available with less complications. The goals are to achieve a good bladder storage/voiding cycle, with low intravesical pressure with maintenance of urinary continence and little or no residual urine. These techniques includes:
  • Behavioral techniques
  • Physiotherapy
  • Intermittent catheterization and intermittent self-catheterization
  • Transurethral and suprapubic catheters
  • Appliances (condom catheters and penile clamp).
 
Behavioral Techniques
Behavioral therapy is important in all patients. It is most valuable in patients with some amount of bladder control and intact bladder sensation. It is helpful in patients like CVA, multiple sclerosis (MS), dementia, Parkinson's, incomplete spinal cord injury (SCI) and transverse myelitis.
  • Timed voiding: Chronic/frequent over distension leads to flaccid, large capacity, permanent paralytic bladder. Timed voiding means maintaining fixed interval between episodes of urination/toileting. The primary goal of timed voiding is to void before urinary urgency and occurrence of incontinence. It is done by frequent voiding to lower the residual urine or by increasing the voiding interval to reduce frequency. This type of “bladder drill” helps to hold more urine and inhibit inappropriate detrusor contractions during the filling phase of bladder
  • Modifying/Adapting drinking habits: Includes balanced fluid intake/restricting caffeinated beverages and bladder irritants. 6Toilet facility should be nearby to the patient which improves the mobility. Planning a fluid schedule is an important initial event in the management. The recommended fluid schedule is 400 cc with meals; 200 cc at 10 AM, 2 PM, and 4 PM; and only sips of fluid after the evening meal (1800 cc/day total). This schedule limits the urine formation about 1500 cc with insensible fluid loss.
Patient is also instructed to keep a voiding diary—helps to know functional bladder capacity, sensation.
 
Physiotherapy
Detrusor over activity from defective central inhibition or increased detrusor afferent activity can be improved by reinforcing inhibitory pathways. Pelvic floor muscle training should benefit patients with weak pelvic musculature. To activate this myotomes a simple technique like standing on tiptoes can suppress urgency.5
The activation of sacral dermatomes particularly glans penis, clitoris and anus can inhibit detrusor activity by enhancing sympathetic neurons and inhibiting preganglionic bladder motor neurons.
The bladder drill for urgency and urge incontinence, consists of teaching the patients to sit down on a rolled-up towel and press on or squeeze the clitoris/glans penis to activate the appropriate dermatomes. This type of training reduces urgency by inhibiting the bladder contraction and increase the functional bladder capacity.
Transcutaneous electrical nerve stimulation over sacral dermatomes (s2–s4) reduces urgency and urge incontinence. Various studies proved that electrode placed over s3 dermatome and stimulation of this electrodes in the range of 2–10 Hz has shown significant positive response in the form of reduction in bladder urgency, improvement in bladder capacity and reduction of bladder pressure compared to pre- stimulation.
  • Physiotherapy for detrusor hypoactivity: Detrusor overactivity can be enhanced by pressing or tapping over the bladder wall which will activate stretch receptors. Other techniques like bending forward and straining can also activate bladder contraction. Pelvic floor relaxation helps bladder emptying.
    Pelvic floor muscle electric stimulation is very useful in patients with DSD with urinary retention. Plevnik et al.6 treated six patients with spinal cord lesions from C5 to T4,using anal or vaginal electrodes monophasic square pulses of 1 ms, frequency of 20 Hz and 50–90 mA, a reduction in maximal urethral pressure was reported.
    Intravesical transurethral bladder stimulation uses the procedure of combining direct stimulation of bladder receptors with visual feedback using patient observance of cystometric pressure changes. It is useful in patients with bladder underactivity due to neuromuscular weakness
  • Triggered reflex voiding: It consists of bladder reflex triggering maneuvers performed by patient to elicit reflex detrusor contractions by external stimuli. These are suprapubic tapping, thigh scratching, squeezing the glans penis and the scrotal skin, pulling on the crines pubis, anal/rectal manipulation. Only in a minority these methods are useful
  • Bladder expression: Comprises various maneuvers like Valsalva (abdominal straining) and the Credé (manual compression of the lower abdomen) maneuvers. These methods are useful in patients with lower motor neuron lesions where combination of an underactive detrusor with an underactive sphincter or with an incompetent urethral closure mechanism of other origin.
 
Catheterization
 
Intermittent Catheterization and Self Intermittent Catheterization
The aim of catheterization is mainly to evacuate the bladder. In NB with partial or complete urinary retention intermittent catheterization (IC) is the technique of choice. Self-administered IC improves patient self-care, independence, decreases barriers to sexual function and daily 7activity. For achieving continence in patient on IC a bladder with adequate capacity, low pressure and a balance between fluid intake, residual urine and catheterization frequency is necessary. If the patient retains some voluntary control, voiding can be attempted at timed intervals or when the urge occurs. Intermittent catheterization partly aids in bladder retraining by gradually decreasing residual urine. Complications includes bacteriuria and urinary tract infection (UTI), urethritis, epididymitis, epididymorchitis, prostatitis, urethral trauma, hematuria, urethral false passages, strictures etc. Asymptomatic bacteriuria is a common finding.
In patients whom IC is not feasible, indwelling catheter may be used. This can be urethral catheter or suprapubic catheter. Commonest complication during indwelling catheter are UTIs but in a long term care setting prophylaxis against UTI is usually not advised.
Fluid intake should be generous in patients with indwelling Foleys catheter or suprapubic catheter. Long term catheterization produce bacterial colonization (biofilm) particularly at the catheter tip. Urease producing organisms elevate pH and cause calcium magnesium phosphate crystals leading to catheter obstruction. This produces or aggravates urinary tract infection. To prevent this complications urine pH must be kept alkaline (pH 8), combined with liberal fluid intake (total intake 3L/day). Increasing dietary citrate (fruit juices) to at least 11 g/day helps to keep urine pH 8 in conjunction with increasing fluid intake. Suprapubic catheter has many advantages.
  • Easy to maintain catheter and hygiene
  • Less tendency to kink
  • Less interference with social functioning like sexual activity
  • Urethral injury like erosion avoided.
 
Suprapubic Cystostomy
This technique is mainly used in patients with poor upper extremity dexterity, as well as the presence of DSD. Other potential candidates include patients with extensive urethral damage or in whom other methods are impractical. Although open suprapubic cystostomy under anesthesia is the definitive gold-standard approach, many less invasive techniques are also available.
 
Appliances
Condom catheters have a role in male patients with NB for short term management. In the long run, their use may lead to bacteriuria. If applied properly complications are less. In this method frequent change of condom, maintenance of good hygiene, and low bladder pressure is essential. Complications like skin maceration and ulcers may develop but compared with urethral catheters there is low incidence of infections.
 
PHARMACOLOGIC THERAPIES FOR NEUROGENIC BLADDER (TABLES 3 AND 4)
Many drugs are available for NB, these include:
  • Antimuscarinics
  • Alpha-blockers
  • Tricyclic antidepressants.
Most commonly used are antimuscarinics, mostly administered orally, rarely as intravesical instillation.
 
Antimuscarinics
Antimuscarinic drugs are the first-line drugs for patients with NB/neurogenic detrusor overactivity (NDO).
Table 3   Antimuscarinic drugs
Medication
Dosage
Oxybutynin
2.5– 5mg/day 2–4 times/day
Oxybutynin extended release
5–30 mg once daily (OD)
Tolterodine
1–2 mg two times a day (BD)
Tolterodine extended release
2–4 mg OD
Darifenacin
7.5–15 mg OD
Solifenacin
5–10 mg OD
Trospium chloride
20 mg BD
Trospium chloride extended release
60 mg OD
8
Table 4   Other drugs used in neurogenic bladder
Drug
Remarks
Therapeutic use
Side effect
Cholinergic agonists: Urecholine
Administered 1 h before bedtime with voiding attempt by manual technique
Promote detrusor contraction in mixed type of NB
Hypotension, bradycardia, bronchospasm abdominal cramps
Alpha 2 adrenergic agonists :
Clonidine, tizanidine
Tizanidine oral
Clonidine: Oral and transdermal
For reducing bladder outflow resistance and also reduce pain and skeletal muscle tone
Fatigue, dizziness, dry mouth constipation
Alpha 1 adrenergic antagonists: Dibenzyline, terazosin, t Tamsulosin, alfuzosin
Reduces urinary outflow resistance by post synaptic block
May produce headache, light headedness
Benzodiazepines: Diazepam
(potentiate the inhibitory neurotransmitter GABA)
To reduce external urinary sphincter spasticity in UMN or mixed lesions
Sedation, delirium, respiratory depression, constipation. Can produce dependence
GABA-B agonists: Baclofen
Modulation of GABA-B receptors at spinal and supraspinal level
Can be administered intrathecally
To reduce external urinary sphincter spasticity
Excessive sedation, no dependence compared to diazepam
Vanilloids: Capsaicin/RTX (resiniferatoxin)
Reduces detrusor over activity by desensitizing the unmyelinated c fiber which transmit urothelial pain
Reduces detrusor hyperreflexia in spinal cord lesion
Clinical use is limited because of lack of stability of vanilloid solutions
GABA, gamma-aminobutyric acid; NB, neurogenic bladder; UNM, upper motor neurons.
Acetylcholine is the neurotransmitter involved in detrusor contractions, antimuscarinics inhibit at muscarinic receptor level leading to relaxation of detrusor and improved storage. This results increased bladder capacity and reduced urgency to void.
Oxybutynin is available as immediate, sustained-release oral preparations, transdermal and topical gels. Tolterodine tartrate and trospium chloride are available both immediate, and sustained-release oral formulation. Since these drugs doesn't cross blood-brain barrier they produce less cognitive side effects and dry mouth than oxybutynin.7
Overall, antimuscarinic therapy can provide substantial benefits to patients with NB and NDO. A recent meta-analysis that included a total of 960 patients with NDO in 16 randomized clinical trials (RCTs) found that antimuscarinics were associated with statistically significant better patient-reported cure or improvement, higher maximum cystometric capacity, higher volume at first detrusor contraction and lower maximum detrusor pressure when compared with placebo. Of all these drugs studied and found to be effective no one drug is superior over other. The side effects include dry mouth, constipation, nausea, and visual disturbance.
Combination therapy is considered when monotherapy has failed. Combination of two antimuscarinics at high-dosage was found to be useful when one agent has failed.
 
Tricyclic Antidepressant Drugs
Introduced for depressive treatment, their side effect made them second line agents. The 9anticholinergic side-effects of this class of drugs have been used to reduce bladder detrusor tone in neurogenic bladder dysfunction. Imipramine has strong anticholinergic effects, so it reduces bladder tone, increases internal sphincter tone which will facilitate urine storage. Amitriptyline is also used some times.
 
Botulinum toxin
A naturally occurring neurotoxin, derived from clostridium botulinum bacterium which produce flaccid paralysis of striated muscle by blocking presynaptic release of acetylcholine. Even though many type of botulinum toxin are available commercially, for urological condition onabotulinumtoxinA (BoNT/A) is the FDA-approved one.8
The toxin has effect mainly on efferent muscle contraction, with possible afferent effects on bladder function as well.
Injection of BoNT/A into the detrusor muscle produce dose-dependent muscle relaxation due to reduced neural signal transmission. The BoNT/A's effect on bladder smooth muscle is significantly longer than skeletal muscle. Multiple studies confirmed its effect on NB, urinary incontinence, and QoL in MS and SCI patients. At present BoNT/A is approved for patients with detrusor over activity and patients who have poor response to antimuscarinic drugs. The doses used are 200 U to 300 U. Between the used doses both are well tolerated and equally effective. The commonest adverse effect is urinary infections and urinary retention. Increased risk of retention is seen in patients who didn't perform interstitial cystitis at baseline. A dose of 200 U is commonly used because of less adverse effects.9
 
SURGICAL INTERVENTIONS IN NEUROGENIC BLADDER (TABLE 5)
When pharmacological and conservative managements fail surgical options can be considered. It can be of help in many ways like:
  • Procedure to enhance detrusor storage
  • Procedure to enhance emptying
  • Bladder sphincter procedure to restrict emptying
  • Bladder sphincter procedure to enhance emptying.
Table 5   Surgical interventions
Mechanism
Use
Remarks
Complication
Neuromodulation
Enhance detrusor storage by stimulation of Sacral nerve root
Neurogenic Detrusor over activity
Longp-term efficacy is not proved
Lead migration and pain at site of implant
Enterocystoplasty
Enhance detrusor storage by anastomosing ileum or ileocecal segment to detrusor
To increase reservoir and reduce detrusor pressure
Most accepted method for achieving adequate reservoir with success rate of 95%
Infection, anastomotic leaks, enteric or urinary fistulas, strictures
Urinary diversion
Procedure to control detrusor emptying
Patient with NB who have Impractical self-catheterization. Abdominal stoma is created is for clear IC
Major Abdominal surgery
Sphincterotomy
Enhance emptying
Reducing urinary outlet obstruction. DSD with hydronephrosis, VUR. Recurrent UTI due to poor bladder emptying. Usually reserved for quadriplegic male
Fewer UTI Incidence, 50% success rate
Haemorrhage during surgery, erectile dysfunction In males, urethral stricture
IC, intermittent catheterization; UTI, urinary tract infection; VUR, vesicoureteral reflux.
10
Table 6   Future developments
Procedure
Technique
Usefulness
Lumbar to sacral nerve rerouting
Restoring bladder function in spina bifida by creation of a skin-central nervous system bladder reflex arc via lumbar (L5 motor) to sacral (S3) nerve rerouting
  • Success rate of 87% in 110 children in China
  • One-year results of the first North American trial were reported, with 7/9 (87%) of spina bifida
Spinal cord regeneration with fibroblasts transplantation
Transplantation of neuronal and glial precursors into the spinal cord lesions in experimentally induced rats
Reported to result in decreased detrusor pressures and less frequent detrusor hyper reflexia episodes
Implantation of neurotrophin- secreting Schwann cells into rat spinal cord lesions
Implantation of neurotrophin-secreting Schwann cells into rat spinal cord lesions one hour after induced thoracic cord injury
Improved bladder morphology and bladder capacity-Park et al.10,11
Olfactory ensheathing cells (OECs)
Glial cells derived from the olfactory placode, have axonal growth promoting properties in their interaction with astrocytes
In a pilot study of 30 human subjects with chronic paraplegia or tetraplegia, Lima et al.12 transplanted olfactory mucosal cell auto grafts into the area of prior cord damage with at least 1-year (and average of over 2-year) follow up. American Spinal Cord American Spinal Cord Injury Association scores improved in 11 subjects but declined in one, and urodynamic responses were reported improved in five subjects
Some future developments in management is summarized in table 6.
 
CONCLUSION
Neurological disorders often cause bladder and bowel dysfunction. Most patients with NB need long term or even life-long care for optimal life expectancy and QoL. Timely recognition and treatment are essential to prevent upper and lower urinary tract damage. Evaluation of NB include detailed history, neurological assessment and appropriate investigations including urodynamic study. The neurourological management must be individualized to the patient's needs which often requires multi-disciplinary approach. Before major surgical intervention noninvasive and conservative therapies must be tried. Individual's sexual and fertility function should not be ignored.
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