Neurosurgery notes/Bladder

Bladder

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Bladder, bowel, sexual function
RAG
RAG
MCQ
MCQ

Normal

Anatomy

  • Urine is expelled via the urethra via contraction of the detrusor smooth muscle, on the outer wall
  • Bladder
    • Wall has 3 layers
      • Inner longitudinal
      • Outer longitudinal
      • Intermediate circular
    • Urothelium
      • Has 3 layers
      • Inner most layer
      • A sensory organ
      • Releases
        • Neurotransmitters
        • Peptides
        • Neurotrophics
      • Has sensory and cholinergic receptors
    • Suburothelium
      • A dense network of sensory nerve fibres
      • Alpha delta fibres
      • Express mechano-sensation receptors
  • Normal capacity is 400-500 mls, takes 30 seconds to void 5-6 times per day

Peripheral efferent pathways

Sympathetic innervation
  • Origin
    • Intermediolateral cell column T11-L2.
  • Nerve
    • Hypogastric nerve
  • Neurotransmitter
    • Sympathetic postganglionic terminals (hypogastric nerve) release norepinephrine
  • Pathway:
    • Intermediolateral cell columns T12–L2 → hypogastric nerve → β3 receptors in detrusor (bladder relaxation, storage) and α1A/D receptors in urethral smooth muscle/prostate (outlet contraction).
  • Function
    • Causes stop peeing
      • Contractions of the
        • Urethral internal sphincter
        • Bladder neck
      • Inhibition of the detrusor
Parasympathetic efferent
  • Origin
    • Intermediolateral column of S2-S4
  • Nerve
    • Pelvic nerve
  • Neurotransmitter
    • Release of Ach → Acts on M3 muscarinic receptors → Provokes detrusor contraction
  • Pathway:
    • Intermediolateral cell columns S2–S3 (sacral parasympathetic nuclei) → pelvic splanchnic nerves → cholinergic terminals in detrusor (M2/M3) → bladder contraction and voiding.
    • Represents the main excitatory input into the bladder
  • Function
    • Allows peeing
Somatic motor nerves
  • Nerve
    • Pudendal nerve
  • Origin
    • Arise from S2-S4 motor neurons in Onufs nucleus
  • Innervate
    • External striated urethral
    • Anal sphincter
    • Pelvic floor muscles
  • Pathway
    • Anterior horn cells including Onuf’s nucleus S2–S3 → pudendal nerve → nicotinic receptors in external sphincter → voluntary sphincter contraction and guarding reflex.
  • Function
    • Voluntary control of bladder
Efferent innervation TIO Tll T12 SYMPATHETIC Hypogastric plexus Hypogastric Detrusor muscle BLADDER PARASYMPATHETIC Pelvic nerves (nervi erigen tes) Hypogastric Spinal cord L2 L3 V nerve Inferior hypogastric ganglion Spinal cord Internal sphincter External sphincter plexus Pudendal nerves Function: Detrusor muscle relaxation Internal sphincter contraction SOMATIC EFFERENT Origin: anterior horn cells S2, 3, 4 — Voluntary innervation CORTICAL CONTROL Frontal lobe: paracentral lobe — initiates micturition — inhibits micturition Afferent innervation 10 11 12 2 Spinal cord SYMPATHETIC Enter through posterior rami and terminate in anteromediolateral column T9—L2 BLADDER Hypogastric plexus 0 The afferent pathways are responsible for the sensation of bladder fullness Function: Detrusor muscle relaxation Internal sphincter contraction PARASYMPATHETIC Pudendal nerve Enter through posterior rami and terminate in anterolateral column, Function: Sensation of painful distension conveyed from bladder wall Function: Sensation of pain and distension conveyed from bladder wall and internal sphincter
notion image
Spinal cord TIO-L2 Hypogastric S2-S4 Sacral micturation centre Cerebral cortex (interprets messages as full or empty bladder) Pontine micturation centre (switches between filling/storage & voiding) Hypogastric nerve (sympathetic) (inhibits detrusor contraction during filling mode & contracts muscles in urethra & bladder neck) Pelvic nerve (parasympathetic) (unopposed impulses make detrusor contract) Pudendal nerve (somatic) (under voluntary control) Voluntary muscle Bladder Pelvic floor External sphincter
Afferent Viceral/EUS Cutaneous perineal Muscle spindle Genital/visceral overlap Kissauer's tract LCP Efferent SPN (Spinal parasympathetic nucleus) MCP Onuf's nucleus Levator ani motor neurons
 

Peripheral afferent pathways

  • Pathway
    • Bladder/urethral mechanoreceptors → Alpha delta fibres (in suburothelium) are sensitive to mechanical stimuli → pelvic, hypogastric, pudendal afferents → dorsal roots of lumbosacral and thoracolumbar cord.
      • Dorsal pathways: spinal cord dorsal tracts → brainstem and higher centres (first sensation of filling, normal desire) → Ascend and synapse on the periaqueductal grey (PAG) and are then relayed via the hypothalamus and thalamus to the
        • Dorsal anterior cingulate cortex
        • Right insula
        • Lateral prefrontal cortex
      • Spinothalamic tract: spinal cord → thalamus and cortex (urgency, pain).
  • Storage phase
      • The medial prefrontal cortex is active and is inhibited by the thalamus, this causes the Medial prefrontal cortex (MPFC) to inhibit the PAG; which in turn inhibits the Pontine Micturition centre (PMC)
      Prefrontal cortex r ront Ventromedial prefrontal cortex Amygdala x
  • Voiding phase
      • The MPFC relaxes its inhibition of PAG and the hypothalamus also provides a 'safe' signal;
      • Consequently the PAG excites the PMC which in turn sends descending motor output to the sacral spinal cord
      • Process of voiding
        • The first aspect of voiding is the relaxation of the striated urethral sphincter
        • This is followed by a contraction of the detrusor which is sustained until emptying is achieved
        • This coordination of relaxation of contract (the opposite being the case in storage) depends on intact connections between the OMC and the sacral spinal cord
      Pontine Mi«turition Center Pontine storage center + Contracts bladder outlet — Inhibits detrusor Hypogastric nerve PAG Pontine micturition center Contracts detruso — Inhibits bladder outlet Hypogastric nerve Urinary bladder Pelvic nerve Pudenal nerve Urinary bladder Pelvic nerve Pudenal nerve External sphincter O External sphincter

Phase switch: storage → voiding

  • Rising volume:
    • Bladder distension → pelvic afferents → spinal cord → PAG; PAG integrates with PFC, insula, cingulate, hypothalamus.
  • Behavioural permission:
    • PFC decision signals → insula/cingulate + hypothalamus → PAG shifts to “voiding” → PMC activated, pontine storage centre suppressed.
  • Final execution:
    • PAG (voiding state) → PMC → reticulospinal tract → sacral parasympathetic activation + pudendal inhibition + sympathetic reduction → high-pressure detrusor contraction against an open outlet → voiding.
 

Spinal cord centres and reflexes

  • Sacral spinal cord S2–S4:
    • Sacral parasympathetic nuclei → pelvic nerves (bladder and urethra).
    • Onuf’s nucleus (anterior horn) → pudendal nerve (external sphincter).
  • Thoracolumbar T12–L2:
    • Intermediolateral cell columns → hypogastric nerve (bladder and urethra).
  • Storage reflex arc:
    • Bladder filling → pelvic afferents → sacral spinal interneurons → activation of sympathetic (hypogastric) and somatic (pudendal) efferents → detrusor relaxation + outlet contraction.

Brainstem centres

  • Afferents to midbrain: spinal afferents → dorsal horn → dorsal and spinothalamic pathways → periaqueductal grey (PAG, “on–off” switch).
  • PAG → pons: PAG → pontine micturition centre (PMC) and pontine storage centre (L-region).
  • Voiding pathway: PAG (voiding mode) → PMC → descending reticulospinal fibres (medial to pyramids) →
    • Excite sacral parasympathetic nuclei → pelvic nerve → detrusor contraction.
    • Inhibit Onuf’s nucleus → pudendal nerve → external sphincter relaxation.
    • Reduce thoracolumbar sympathetic outflow → hypogastric nerve → internal sphincter relaxation, loss of β3-mediated detrusor relaxation.
  • Storage pathway: higher centres (PFC–insula–cingulate–hypothalamus–PAG) → pontine storage centre → tonic excitation of sympathetic and pudendal outflow, suppression of parasympathetic voiding.

Suprapontine storage control

  • Ascending sensory route: bladder filling → pelvic/hypogastric/pudendal afferents → spinal cord → PAG → insular cortex and anterior cingulate → prefrontal cortex.
  • Main cortical–subcortical loop (storage):
    • Bladder filling → spinal afferents → PAG → insula/anterior cingulate → prefrontal cortex → hypothalamus → PAG → pontine storage centre → spinal sympathetic and somatic centres → detrusor inhibited, outlet activated.

Basal ganglia modulation

  • Nigrostriatal pathway: substantia nigra pars compacta → dopamine to striatum (D1/D2) → direct and indirect basal ganglia pathways → output nuclei (GPi, SNr) → GABAergic projections to brainstem micturition circuit.
    • Substantia nigra pars compacta (SNC)
      • SNC dopaminergic neurons → striatum (putamen and caudate).
      • Dopamine acts on D1 and D2 receptors in the striatum.
    • Direct (D1) pathway – main bladder‑inhibitory route
      • SNC dopamine → D1 receptors in striatum → activation of D1‑GABAergic direct pathway.
      • Striatum (direct pathway) → GABAergic inhibition of basal ganglia output nuclei (globus pallidus pars interna, GPi; substantia nigra pars reticulata, SNr).
      • GABAergic collaterals from this circuit also project to the micturition circuit and inhibit the micturition reflex.
      • Net effect of D1 pathway: facilitates urinary storage by inhibiting the micturition reflex.
    • Indirect (D2) pathway – more complex, partly facilitatory
      • SNC dopamine → D2 receptors in striatum → modulation of the indirect GABAergic pathway via globus pallidus pars externa and subthalamic nucleus.
      • Subthalamic nucleus → excitatory (glutamatergic) drive to GPi/SNr, which in turn influence the micturition circuit.
      • High‑frequency stimulation (functionally inhibitory) of the subthalamic nucleus → bladder inhibition (reduced detrusor overactivity).
    • Interaction with brainstem micturition circuit
      • Basal ganglia output nuclei (GPi/SNr) → GABAergic projections to midbrain/brainstem micturition centres (PAG and pontine micturition centre).
      • Through these projections, dopamine‑dependent basal ganglia activity modulates PAG–PMC control of the sacral spinal micturition reflex.
  • Storage bias: nigrostriatal dopamine (mainly D1) → activates direct pathway → inhibits basal ganglia output → GABAergic collaterals inhibit micturition reflex circuits → promotes storage/suppresses voiding.
    • Loss of D1‑mediated inhibition (for example, Parkinson disease) → reduced basal ganglia inhibition of micturition circuit → disinhibited micturition reflex → detrusor overactivity and OAB.
Micturition circuitry
Micturition circuitry
Basal ganglia–dopamine control of micturition
Basal ganglia–dopamine control of micturition

Dysfunction

General

  • “Brain (suprapontine) → OAB / detrusor overactivity.”
  • “Spinal cord / cauda / peripheral → underactive bladder, DSD, mDO–DU, large residuals, high‑pressure risk.”

Lesion location

Supra-pontine
  • Many cortical and subcortical diseases impair the normal inhibition of the PMC that is needed for voluntary micturition
    • The paracentral lobule in NPH is damaged this causes loss of inhibition of bladder and bowel voiding
  • Frontal lobe pathology can cause urge incontinence
  • Often the process of voiding is not affected so raised post void >100 mls is not expected
Spinal Cord
  • Loss of connection between PMC and sacral cord
  • Results in reflex bladder contractions in response to low volume filling
  • Known as Detrusor-Sphincter-Dyssynergia (DSD) and leads to high intra bladder pressure and renal damage
  • Real risk of this following spinal cord injury (hence importance of a catheter)
Sub-sacral
  • Lesions of the cauda equina often cause a hypo contractile detrusor
  • This results in voiding difficulty, weak flow, incomplete emptying and retention, there may also be decreased bladder sensation due to efferent interruption
  • The precise picture depends on whether the post ganglionic fibres are affected
    • If they are intact (as in sacral root damage) some reflex balder activity can still occur, sphincter denervation is expected if there has been damage to the sacral roots
      •  
notion image

Brain diseases

  • Stroke
    • Basal ganglia / internal capsule / frontal micturition centre.
    • Acute: possible detrusor underactivity; chronic: detrusor overactivity → OAB, urgency ± incontinence.
  • Alzheimer disease
    • Temporoparietal and frontal cortex, central cholinergic loss.
    • Storage disorder: OAB (detrusor overactivity) in up to ~40% once other causes excluded.
  • White matter disease (WMD)
    • Diffuse subcortical WM, frontal connections.
    • Early, prominent OAB; detrusor overactivity often precedes gait/cognitive decline.
  • Normal‑pressure hydrocephalus
    • Frontal hypoperfusion, subcortical fibre disruption.
    • OAB with urgency/frequency ± incontinence; detrusor overactivity correlates with PFC hypoperfusion.
  • Parkinson disease
    • Nigrostriatal dopamine loss; also cholinergic and serotonergic depletion.
    • OAB in ~70%: detrusor overactivity from loss of D1‑mediated inhibition of micturition reflex.
  • Dementia with Lewy bodies (DLB)
    • Widespread cortical + subcortical Lewy body pathology.
    • OAB in ~90%, usually more severe than PD (combined cortical + dopaminergic lesion).
  • Multiple system atrophy (MSA)
    • Basal ganglia, pons, cerebellum, lumbosacral cord (IML, Onuf, lumbar IML).
    • Classic mDO–DU ± DSD: OAB + large residuals / retention; open bladder neck, abnormal sphincter EMG.

Spinal cord diseases

  • Complete supra‑sacral SCI
    • Descending micturition pathways interrupted.
    • Early (spinal shock): detrusor underactivity (areflexic bladder).
    • Later: detrusor overactivity + DSD → high‑pressure bladder, large residuals, reflux, risk of autonomic dysreflexia.
  • Incomplete SCI
    • Partial cord lesions (e.g. Brown‑Séquard, spondylotic).
    • mDO–DU ± DSD: OAB with hesitancy/weak stream and significant residuals; storage and voiding phases still partly separable.
  • Multiple sclerosis (MS)
    • Multifocal CNS, often incomplete spinal cord lesions.
    • >60% detrusor overactivity (OAB); up to ~20% detrusor underactivity; up to ~46% mDO–DU with DSD.
  • Neuromyelitis optica spectrum disorder (NMOSD)
    • Longitudinally extensive myelitis.
    • LUTS more severe than MS: DO, DSD, sometimes autonomic dysreflexia; storage and voiding both affected.
  • Spina bifida – cystic
    • Malformed lumbar/sacral cord and roots.
    • mDO–DU very common: DO, low compliance, DSD, DU → high‑pressure voiding, large residuals, reflux, hydronephrosis, incontinence.
  • Spina bifida – occult
    • Occult lumbosacral malformation (tethered cord, lipomeningocele, etc.).
    • Variable NLUTD: from nocturnal enuresis to retention; often mDO–DU with impaired sensation and DSD.

Management

General principles

  • Take detailed history, use LUTS questionnaires and a 3‑day bladder diary.
  • Perform neurological examination, renal function tests and urinary tract imaging.
  • Do (video)urodynamics where possible to define pattern (OAB, DU, mDO–DU, DSD).
  • Always consider motor and cognitive causes of incontinence (immobility, dementia).

Step 1: Find and treat common comorbidities

  • Benign prostatic hyperplasia (men >50):
    • Check with ultrasound and/or cystoscopy; confirm obstruction with pressure–flow or videourodynamics.
    • Treat with α‑blockers, 5‑α‑reductase inhibitors, PDE‑5 inhibitors, minimally invasive procedures or surgery.
  • Pelvic organ prolapse / stress incontinence (women >50):
    • Diagnose by inspection and history; if equivocal, use chain urethrocystography and stress videourodynamics.
    • Treat with pelvic floor exercises, pessaries, and/or surgery.
  • Polyuria / nocturnal polyuria:
    • Detect on 3‑day diary (polyuria >3 L/day; nocturnal >33% of 24‑h volume).
    • Evaluate for cardiac/renal disease; recognise loss of nocturnal AVP rise in some neurological diseases.
    • Manage with fluid‑timing, increased walking and oral or nasal desmopressin with sodium monitoring.
  • Neurological comorbidities causing DU:
    • Recognise diabetes neuropathy and lumbar spondylosis/cauda equina neuropathy as causes of detrusor underactivity and residuals.

Step 2: Maintain safe pressure and efficient emptying

  • High vesical pressure (e.g. SCI, advanced MS, spina bifida):
    • Check kidneys (blood/urine tests) and perform urodynamics.
    • Treat high pressure using the same strategies as for OAB (see storage management).
  • Post‑void residual surveillance:
    • Measure residuals regularly in patients at risk of DU or mDO–DU (peripheral neuropathies, spinal cord disease, MSA), using portable bladder ultrasound, abdominal ultrasound or catheterization.
  • Large residuals / underactive bladder (DU, mDO–DU):
    • First‑line: clean intermittent catheterisation (CIC) taught to patient or caregiver by clinicians or specialist nurses.
    • CIC can be done even with some hand impairment (e.g. C5–C6 SCI) using braces/attachments; feasible in older people unless severe cognitive decline.
    • If CIC is not possible: use an indwelling catheter (transurethral, suprapubic cystostomy or ileal conduit), accepting higher long‑term complication rates (infection, bladder cancer).

Step 3: Treat storage symptoms / detrusor overactivity (OAB, high pressure)

  • Use standard OAB pharmacotherapy to reduce detrusor overactivity and intravesical pressure (antimuscarinics, β3‑agonists as per cited guideline).
  • Apply this to:
    • OAB due to brain lesions (stroke, Alzheimer disease, white matter disease, normal‑pressure hydrocephalus, Parkinson disease, dementia with Lewy bodies).
    • The storage component of mixed DO–DU in conditions such as multiple system atrophy, multiple sclerosis, spinal cord injury, neuromyelitis optica spectrum disorder and spina bifida.

Step 4: Treat voiding failure / detrusor underactivity

  • For DU or mDO–DU with significant residuals:
    • Core strategy is assisted emptying (CIC preferred).
    • Use long‑term indwelling catheters only when CIC is not possible.
    • Avoid high‑pressure straining voids.
    • Correct coexisting outlet obstruction (BPH, pelvic organ prolapse) as in step 1.