Gait disorders


Gait, parkinsonism, festinating gait, abnormal gait

Gait depends on both maintenance of equilibrium and mechanisms of locomotion. Abnormal gait, especially in the elderly, is due to a combination of factors. A useful approach to assessing contributors to gait disorder is by localizing the level of the sensorimotor deficits and differentiating them into three groups: low, middle, and high sensorimotor level gait disorders, as shown in Table 67.

Low sensorimotor level gait disorders can be divided into peripheral sensory or peripheral motor dysfunction. In peripheral sensory impairment, an unsteady and tentative gait is commonly caused by vestibular disorders, peripheral neuropathy, proprioceptive deficits, or visual ataxia. Peripheral motor impairment results from arthritic, myopathic, and neuropathic conditions that cause deformity of the extremities, painful weight bearing (e.g., antalgic gait), and focal weakness (e.g., Trendelenburg gait in hip adductor weakness and “steppage” gait in foot drop). The resulting gait disorders are primarily compensatory, allowing patients to adapt well to the deficit.

Middle sensorimotor level gait disorders encompass hemiplegic, paraparetic, cerebellar ataxic, parkinsonian, choreic, hemiballistic, and dystonic gaits. Pyramidal, cerebellar, and basal ganglia motor systems dysfunction results in faulty execution of centrally selected postural and locomotor responses, resulting in the disruption of the sensory and motor modulation of gait. Despite the abnormal stepping pattern, gait initiation and postural reflexes are usually intact. Gait freezing is often seen in Parkinson disease, particularly when making a turn or going through a doorway. Other clinically significant aspects of the parkinsonian gait include decreased stride length, postural instability, and festination (slow, shuffling steps that slowly increase in speed, predisposing a forward fall).

High sensorimotor level gait disorders have more nonspecific gait characteristics. They are due to difficulties in frontal planning and execution, including cautious gait, frontal and subcortical disequilibrium, gait ignition failure (gait apraxia), frontal gait disorders, primary progressive freezing gait disorder, and psychogenic gait disorder. Simply holding a patient lightly by the finger during the neurologic exam can help to diagnose disorders of gait initiation. Cognitive dysfunction and behavioral aspects, such as fear of falling, play a role, particularly in cautious gait. The severity of frontal-related disorders runs a spectrum from gait ignition failure to frontal gait disorder to frontal disequilibrium, in which gait initiation difficulty and small shuffling steps progress to the point at which an unsupported stance is not possible. They are difficult to differentiate clinically and are usually the result of a lesion that affects the corticobasal ganglionic-thalamocortical loop, caused by bilateral infarction, hemorrhage, neoplasm, hydrocephalus, or a degenerative process.

Gait disorder in the elderly frequently results from an overlap of deficits in the three sensorimotor levels. Two mechanisms appear to precipitate gait disorders, particularly in the elderly. First, “benign disequilibrium of the elderly” is a multiple sensory deficit syndrome (a combination of impairments in position and tactile sense, vision, hearing, and vestibular or baroreceptor function) causing vague dizziness or disequilibrium (“dizziness of feet”) while standing, walking, or turning, but not while sitting or lying. Equilibrium improves by holding or leaning onto a wall. These patients benefit from gait training and use of an assistive device (cane or walker) and should not be medicated (meclizine, benzodiazepines) for presumed vestibular disease. A second common problem is acute deterioration in gait, balance, and postural adjustments in acutely ill, elderly patients. The ensuing “toxic-metabolic encephalopathy,” caused by medications, organ failure, dehydration, electrolyte imbalance, or systemic infection, may result in varying gait difficulty and altered postural reflexes, gegenhalten (paratonia involving an involuntary resistance to passive movement) of limb and neck, diffuse myoclonus, and bilateral asterixis. Acute gait disorder may in turn be the presenting feature of acute systemic decompensation in the elderly and warrants further evaluation (i.e., stroke, myocardial infarction, or infection).

Diagnosis of gait disorders is based on history and associated neurologic findings. Isolated gait disorders in the elderly are frequently due to treatable disorders such as Parkinson disease, cervical myelopathy, or normal-pressure hydrocephalus. Gait evaluation and training by physical therapy should be initiated early. Discontinuing unnecessary medication use and home safety evaluations are pertinent in preventing future falls.


Fung V.S. Functional gait disorder. Handb Clin Neurol. 2016;139:263–270.

Pirker W., Katzenschlager R. Gait disorders in adults and the elderly: a clinical guide. Wien Klin Wochenschr. 2017;129(3-4):81–95.

Gaze palsy


Diplopia, oculomotor nerve, abducens nerve, trochlear nerve

Horizontal gaze palsies

A unilateral gaze palsy (for both saccadic and pursuit movements) may indicate a contralateral cerebral hemispheric (frontoparietal), contralateral thalamus, midbrain, or ipsilateral pontine lesion. Except when the pontine lesion is at the level of the abducens nucleus, either involving the nucleus itself or the paramedian pontine reticular formation, the eyes can be driven toward the side of the palsy with cold caloric stimulation of the ipsilateral ear or oculocephalic maneuvers. Hemispheric lesions characteristically produce transient defects; brainstem lesions may be associated with enduring defects. An acute cerebellar hemispheric lesion can result in an ipsilateral gaze palsy that can be overcome with caloric testing. Unilateral saccadic palsy with intact pursuit is unusual and indicates an acute frontal lesion. Unilateral impaired pursuit with normal saccades is usually due to an ipsilateral deep posterior hemispheric lesion with a contralateral hemianopia.

Vertical gaze palsies

Vertical gaze palsies are harder to localize since there are more muscles innervated by cranial nerves II and IV. The rostral interstitial nucleus of the medial longitudinal fasciculus in the upper midbrain contains the cells that generate vertical eye movements. A medially placed lesion will result in both an up-gaze and down-gaze palsy. An isolated down-gaze palsy is often due to a bilateral or lateral midbrain lesion. Isolated up-gaze palsies occur with lesions of the posterior commissure, bilateral pretectal regions, and large unilateral midbrain tegmental lesions. In the dorsal midbrain syndrome (Parinaud syndrome) the paralysis of upward gaze is usually associated with convergence-retraction nystagmus, lid retraction, and light-near dissociation of the pupils. An acute bilateral pontine lesion at the level of the abducens nucleus may result in a transient up-gaze paralysis in addition to bilateral horizontal gaze palsy.

Conjugate eye deviations

Horizontal deviations are associated with acute gaze palsies as described above and with irritative cerebral foci (seizure or intracerebral hemorrhage), which usually drive the eyes to the side opposite the lesion. Ipsiversive eye and head movements, however, are reported with focal seizures. Tonic upward deviations occur in the oculogyric crisis of postencephalitic parkinsonism and, more commonly, as an idiosyncratic reaction to phenothiazines and other neuroleptics. They may also occur in coma, often anoxic encephalopathy. Downward deviations may occur transiently in normal neonates but also in infantile hydrocephalus and in adults with metabolic encephalopathy, bilateral thalamic infarction, or hemorrhage.

Gerstmann syndrome


Gerstmann syndrome, agraphia, acalculia, finger agnosia, left-right confusion

The clinical tetrad of agraphia, acalculia, agnosia to fingers, and agnosia to right-left (disorientation) defines Gerstmann syndrome. Finger agnosia may manifest as bilateral difficulties in finger naming, moving fingers to command, matching of fingers to demonstration, or recognizing stimuli (“wiggle the finger that I touch”). When all features are present, a dominant inferior parietal or posterior perisylvian lesion is highly likely. People with Gerstmann syndrome usually have other deficits as well, such as aphasia. Alexia and constructional apraxia may also accompany Gerstmann syndrome.

Gerstmann syndrome can also manifest in the context of global disease such as SLE, AIDS, or multiple sclerosis.

In children, developmental Gerstmann syndrome may occur, and the cause is often not known. It may occur with or without dyslexia. Verbal IQ among such children is often significantly higher than performance IQ.

Aug 12, 2020 | Posted by in NEUROLOGY | Comments Off on G
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