Balint Syndrome


Balint syndrome, simultagnosia, optic ataxia, ocular apraxia, parietal lobe, bilateral parietal lesions

Described in 1909 by Reszö Balint, this syndrome consists of a rare triad of simultagnosia, optic ataxia, and ocular apraxia owing to bilateral parietal lesions. As a result, patients present complex visual disturbances, or seem as if blind—unable to integrate visual input from their surroundings—despite preservation of vision. The etiology of Balint syndrome may include stroke, tumor, trauma, neurodegenerative diseases (e.g., Creutzfeldt-Jakob or Alzheimer disease), and HIV infection.

  1. I. Simultagnosia refers to the inability to see the totality of a scene, despite being able to see the individual characteristics of the whole. A diagram showing a familiar scene with people and objects (e.g., the “Boston Cookie Theft,” frequently used in the National Institutes of Health (NIH) stroke scale) can be used to test for simultagnosia. Unlike a normal patient able to describe actions of the objects and people in relationship to each other, someone with simultagnosia may only be able to describe parts of the scene or only parts of objects, but not their relationships to each other. Lesion to the temporo-parietal junction is typically responsible.
  2. II. Ocular ataxia refers to difficulty reaching for objects under visual guidance despite normal limb strength and intact joint position sense. Though typical of bilateral lesions to the parietal lobe, it has been described in unilateral superior parietal lobule lesions independently of Balint syndrome patients.
  3. III. Optic apraxia, described originally as “psychic paralysis of gaze,” refers to an inability to shift gaze voluntarily toward objects of interest despite unrestricted eye movements. This is due to impairment in saccade planning arising from bilateral parietal lesions.

While traditionally Balint syndrome arises from bilateral occipitoparietal lesions, comprehensive reviews suggest that different combinations of lesions in areas deriving from the parietal lobe can yield this presentation. For example, bifrontal lesions resulting in attentional impairment or right hemispheric lesions can produce a neglect syndrome that may mimic Balint syndrome.


Chechlacz M., Humphreys G. The enigma of Bálint’s syndrome: neural substrates and cognitive deficits. J Frontiers in Human Neurosci. 2014;8:1–3.

Rizzo M., Vecera S.P. Psychoanatomical substrates of Bálint’s syndrome. J Neurol Neurosurg Psychiatry. 2002;72:162–178.



Benzodiazepines, dependence, overdose, seizures

Benzodiazepines are used in the treatment of anxiety, insomnia, epilepsy, catatonia, vertigo, and certain movement disorders in addition to management of ethanol withdrawal. Non-parenteral formulations are well known in the acute treatment of epileptic seizures, and intranasal and intramuscular injections are being developed. Prolonged use of any drug in this class may cause physical dependence, particularly in patients with a history of alcohol or substance abuse. Benzodiazepines are one of the top three classes of drugs responsible for death from overdose. Therefore, only the lowest effective doses should be used for the shortest possible period. Side effects include sedation, suppression of rapid eye movement (REM) sleep, amnesia, agitation, and gait disorder. Withdrawal symptoms may occur after 4 to 6 weeks of use and include flulike symptoms, rebound insomnia, irritability, seizures, nausea, headache, tremor, and muscle cramps. In those at risk for withdrawal, the dose should be tapered over several weeks. Acute intoxication with depressed mental status may be reversed with the benzodiazepine receptor antagonist flumazenil, starting at 0.2 mg IV over 30 seconds with a risk of precipitating seizures in the predisposed individual. Failure to respond to a total dose of 5 mg makes it unlikely that sedation is due to benzodiazepines.


Mula M. New non-intravenous routes for benzodiazepines in epilepsy: a clinician perspective. CNS Drugs. 2017;31(1):11–17. doi:10.1007/s40263-016-0398-4.

Rasmussen S.A., Mazurek M.F., Rosebush P.I. Catatonia: our current understanding of its diagnosis, treatment and pathophysiology. World J Psychiatry. 2016;6(4):391–398. doi:10.5498/wjp.v6.i4.391.




Normal bladder function is controlled by bladder stretch receptors (generating sympathetic input to the spinal cord), the bladder wall detrusor muscle (activated by parasympathetic outflow), the internal sphincter (smooth muscle), and the external sphincter (striated muscle under voluntary control). Neural control is mediated by cerebral hemispheric centers (orbitofrontal cortex), the pontine micturition left, the sacral micturition left, and the hypogastric, pelvic, and pudendal nerves (Fig. 9). These centers and nerves work together to achieve: (1) storage of urine without leaking, (2) adequate perception of increased intravesical pressure, (3) release of cortical inhibition of emptying in appropriate circumstances, (4) proper synergy of urinary tract muscular structures, and (5) complete bladder emptying.

Figure 9
Figure 9 Neuroanatomy of bladder control.

Disorders of bladder control can be caused by local factors, such as previous childbirth, pelvic surgery, or urinary tract infection, or disorders of the upper or lower motor neuron (Table 18).

Detrusor hyperreflexia, resulting from cerebral cortical dysfunction, is a deficit of normal inhibitory mechanisms that occurs when the micturition reflex is intact and the lesion is above the pontine micturition left. Symptoms include frequency, urgency, and urge incontinence. Common neurologic disorders leading to uninhibited bladder contraction include stroke, mass lesion, and hydrocephalus.

Bladder dyssynergia, due to suprasacral spinal cord lesions, leads to loss of detrusor-sphincter coordination. Simultaneous contraction of detrusor and sphincter can lead to increased intravesical pressures and upper urinary tract damage. Multiple sclerosis, a spinal cord tumor or trauma, vascular malformation, and herniated intervertebral disc are common causes.

Detrusor areflexia is caused by lesions of the sacral micturition left or its connections to the bladder. Sphincter function is preserved but detrusor contraction is not activated, commonly resulting in overflow incontinence. Causes include myelopathy resulting from a herniated disc or tumor and interruption of the reflex arc as a result of pelvic or pudendal nerve injury following trauma or operation.

Autonomic dysreflexia occurs after spinal cord lesions above the region of major sympathetic outflow (T5–L2). Splanchnic sympathetic outflow is no longer moderated by supraspinal centers, and bladder distention, catheterization, or other manipulation may cause an acute syndrome of severe hypertension, anxiety, diaphoresis, headache, and bradycardia. Prompt recognition and treatment, including blood pressure control and treatment of local bladder problems, are essential.

Table 19 includes agents traditionally used in the pharmacologic management of upper and lower motor neuron bladder dysfunction. Tolterodine (Detrol) is a nonselective antimuscarinic agent which can be used for treatment of detrusor hyperreflexia (symptoms of frequency, urgency, urge incontinence). Its efficacy is equivalent to that of oxybutynin, and it offers the advantages of twice-daily dosing and fewer anticholinergic side effects.

Table 19

Treatment of bladder dysfunction
Upper Motor Neuron Lower Motor Neuron
Treatment goal: increase storage capacity Treatment Increase bladder tone; avoid storage of large urinary volumes; promote bladder emptying
Oxybutynin (Ditropan) anticholinergic
Bethanechol (Urecholine) cholinergic dose:
        Child: 2.5 mg PO bid–tid         Child: 5 mg/day, increase as below
        for adult
        Adult: 5 mg PO tid–qid         Adult: 2.5–10 mg SC tid–qid,
        or 5–50 mg PO tid–qid
Side effects: dry mouth, blurred vision     Contraindicated asthma,
    hyperthyroidism, coronary artery
    disease, ulcer disease
Propantheline bromide (Pro-Banthine) antimuscarinic agent Phenoxybenzamine (Dibenzyline) anti- adrenergic
    Dose:     Dose:
        Child: not currently approved
        for use (USA)
        Child: 0.3–0.5 mg/kg/day

        Adult: 10–30 mg/day
        Adult: 15–30 mg PO tid–qid     Side effects: retrograde ejaculation,
    drowsiness, orthostatic hypotension
    Side effects: dry mouth, blurred vision
Imipramine (Tofranil) mixed anticholinergic and adrenergic
        Child: 1.5–2 mg/kg qid
        Adult: 25 mg PO qid
    Side effects: dry mouth, blurred vision,
    constipation, tachycardia, sweating, fatigue, tremor
Intermittent self-catheterization Intermittent self-catheterization or Credé maneuver

You may also need

Aug 12, 2020 | Posted by in NEUROLOGY | Comments Off on B
Premium Wordpress Themes by UFO Themes