Symptoms Of Arthritis In Hands

Gait Disorders in the Elderly

GAIT DISORDERS: "Doctor, I can't walk"

INTRODUCTION

Walking is easy. We do it all the time without thinking about it. Yet, at any time, if we consciously do pay attention to walking we become aware of our legs and consciously direct the mechanics of ambulation, or gait. When the mechanism for automatic walking breaks down, we refer to the dysfunction as a "gait disorder"

Gait disorders are common: about 15% of people over age 60 have some degree of difficulty with gait and 20-25% of individuals over age 80 use a mechanical aid for walking

The nervous system has to provide for propulsion while maintaining balance and posture. Multiple areas of the brain participate both consciously and unconsciously to directwalking, which makes for complicated physiology. Consequently, as with any complicated electronic device there is the potential for breakdown of any of the components necessary for smooth operation.

Grillner, a pioneer researcher in gait physiology, suggested that three distinct types of control systems are involved. The motor system produces propulsive movements, the postural system maintains appropriate body orientation during ongoing locomotion, and goal directed aspects of behavior bring the organism to the designated goal of the locomotor episode.

Only if the physician is familiar with normal physiology can any attempt be made to pinpoint the site of dysfunction in the nervous system in patients with gait disorders, but with an accurate diagnosis there is the hope of effecting a cure, or at least improvement of function.

Physiology:

The control of walking is a coordinated, multilevel process with participation of multiple areas of the brain and spinal cord gait centers.

Spinal cord:

In both humans and animals a rather ill defined area in the lumbar spine is concerned with walking and this area has been named a spinal locomotor center. A spinal locomotor centers is present also in the cervical regions of animals that walk on all four legs and allows for the coordinated limb movement necessary for walking. These areas, which are not well defined from an anatomical point of view, have been called "central pattern generators." The pattern generators allow for alternate activation and inhibition of the leg muscle. They can function alone in certain circumstances but are normally under the control of higher centers.

The newborn human infant displays "automatic walking", which is due to reflex activation of the lumbar central spinal pattern generator. The soles of the feet are stimulated by planting them on a firm surface. Receptors in the soles and stretch receptors in the tendons, particularly the heel cord, are stimulated and this triggers automatic reflex movements of the legs, and the infant steps forward as though it were walking. The infant may "walk" if the soles are placed on the wall or even ceiling.

In the case of animals, automatic walking movement requires coordination of both fore and hind limbs so that the spinal cord generators must be connected. If a decapitated animal is propped up by its limb girdles and the feet placed on a treadmill, given some chemical priming of the system, the moving treadmill stimulates the foot pads and triggers automatic reflex walking movement. With faster and faster treadmill activity the legs keep up and the animal walks faster and may even trot.

With maturation of the human infant, connections with higher centers are established and the autonomous activity of the spinal cord locomotor center is suppressed as these centers take over Automatic walking cannot be induced after about a month.

Brain stem:

The spinal locomotor centers are under the control of higher centers located in the brain stem, cerebellum, basal ganglia and frontal lobes. The function of these higher centers has been studied in animals by transection experiments, and by electrical and chemical stimulation experiments. Thus, for example, if the brain stem is transected at a specific level, (between the colliculi) extreme spasticity in the limbs can be induced and the limbs are held rigid, sufficient to bear weight. The explanation is that there is release of inherently excitatory nuclei in the brain stem which are normally inhibited by higher centers. Different behaviors can be elicited depending on the level of transection. Any area of the brain stem which, when stimulated induces walking-type movement is, by definition, a brain stem locomotor center; these are multiple and scattered.

Cerebellum:

The cerebellum is connected to the brain stem locomotor centers and is activated synchronously with the various stem nuclei. It receives input from the sensory receptors in the limbs via the ascending spinal cord tracts (spino cerebellar tracts). It, in turn, provides output to the brain stem and higher centers of the brain. The function of the cerebellum is to smooth out movement. Cerebellar activity coordinates timing and adjustment of any particular movement.

Basal Ganglia and Deep Nuclei:

Deep within the cerebral hemispheres are collections of cell nuclei (gray matter)called, the basal ganglia. Different regions have different functions - exploratory locomotion is generated in the basal ganglia, the lateral part of the hypothalamus triggers walking for the purpose of eating or appetitive function, and the medial part of the hypothalamus is active in defensive gait. The caudate is an input nucleus to the basal ganglia and if ablated, cats exhibit a compulsory approach syndrome and walking is stimulus bound so that they walk towards tactile and visual stimuli.

Frontal cortex:

The front part of the brain is the highest locomotor center. It plays a watchful facilitatory role but can take over the whole process at a conscious level.

GAIT DISORDERS:

"Doctor, I can't walk"

The Patient's Experience:

Usually, patients complaining of a gait disorder are elderly, but younger patients, although in the minority, certainly are part of this population.

Most patients try to figure our what is wrong on their own, and the presenting complaint is simply, "I cant walk".The pathophysiology is elucidated only by a careful neurological examination. The patient often suggests weakness, dizziness or lack of balance as the explanation, but because few, if any, patients are armed with an understanding of the basic physiology of ambulation their personal diagnosis is "hit or miss, " frequently "miss."

It certainly is worthwhile for the patient to relate the problems encountered in daily life activities, cognition, or a change in bladder function. These symptoms will help the neurologist figure out what is wrong. Its also worth recording the tempo of the disability - did it come on abruptly as in a stroke, or in a more gradual and progressive fashion? Any associated symptoms could be important and should be recorded.

The Neurologist's Approach:

The neurologist, armed with a knowledge of the physiology sets out by way of the physical examination to pinpoint the neurological deficits, relate them to the physiology, and then establish the cause or pathology that is responsible for the disordered function. This is the one instance in neurological practice where the history is of only limited importance in establishing a diagnosis - the physical examination is all important!

At a basic level there are a number of possibilities to account for dysfunction of ambulation, but the first step is to decide if the deficit is indeed neurological. Pain, arthritis, decreased vision, or shortness of breath could all compromise normal gait and are the rightful territory of the primary care doctor or internist

Disorders of neurologic origin fall into six major categories, defined by.the functional and symptomatic level at which they operate and some patients have a psychogenic dysfunction. Lastly, in any series of gait disorders in the elderly no definite cause can be established and these are labeled "idiopathic".

Basic causes of gait abnormalities:

1. Weakness

2. Deafferentation i.e. Loss of sensory feedback

3. Ataxia i.e. Loss of coordination

4. Dizziness

5. "Extra-pyramidal" dysfunction i.e. dysfunction in the basal ganglia

6. Frontal lobe dysfunction

7. Psychiatric dysfunction

The physical signs and symptoms, and therapeutic approach to each is described below. The diagnosis is dependent on what is found on physical examination. It's a bit like reading a detective novel, rounding up all of the suspects, and then eliminating possibilities one by one in order to finger the culprit. Only after the examination can the physician decide what the best investigative study is for any particular patient.

Weakness

Weakness implies malfunction of muscles which lose their strength. The diagnostic approach here is to decide if the problem is in the peripheral nervous system, or centrally in the brain and/or spinal cord.

The Anatomy:

The peripheral motor nervous system starts in the spinal cord where the cells of origin of the motor nerves (anterior horn cells) are located. The nerve roots connect with the spinal cord by two rootlets; the front or anterior root is motor, for muscle activity, and the posterior or dorsal root is for sensory input. Motor impulses leave the spine via the nerve root. The roots, having exited the boney spinal column, coalesce to form a plexus or network fairly close to the spinal column. One plexus is in the neck, just above the collar bone (clavicle), and the other is in the back part of the lower abdomen. Individually named nerves emerge from the plexus and course to the peripheral muscles in a preordained fashion so that each nerve supplies a particular group of muscles. The termination of each motor nerve is in the muscle and the end of the nerve forms a small disk or plate-like structure called an "endplate." The electrical activity of the nerve is translated into a neurotransmitter chemical (acetylcholine) which is released from the endplate of the nerve, passes into a small cleft-like space between the endplate of the nerve and the muscle itself (synaptic cleft) and activates receptor areas on the muscle surface (post synaptic membrane). This chemical transmission once again triggers electrical activity in the muscle, which contracts.

In LMN weakness the electrical impulses in the nerve fail to reach the muscle because of trouble with the nerve itself, problems transferring the signal through the synaptic cleft, or because there is an intrinsic problem with the muscle itself so that it fails to contract efficiently

The Examination:

The diagnosis of LMN weakness is based on atrophy of the muscle, flaccidity or loss of tone, and by the distribution of weakness. Each root supplies a certain set of muscles, and each nerve supplies a certain set. More diffuse problems with the motor nerves results in more diffuse but distal weakness. If the foot extensors at the ankle are very weak a "foot drop" is seen. The tendon reflex at the ankle may be absent and the plantar response (Babinski) is normal: the toes flex when the sole is scraped.

Characteristic Gait:

The gait is high stepping, to clear the toes from dragging on the ground with each step. This accommodation occurs because the hip flexor muscles are normal and can lift the leg higher than normal. The foot comes down on the ground with a slapping sound or sensation.

The Anatomy:

The UMN starts in the cells of the frontal cortex and the descending motor tracts travel downward through the white matter of the brain, gathering together as the tract passes through the basal ganglia (internal capsule) on its way to the brain stem and thence to the medulla. Here the tracts cross (pyramidal decussation) and enter the spinal cord laterally to terminate around the anterior horn cells.

The Examination:

The diagnosis of UMN weakness is based on increased tone or stiffness (spasticity), absence of muscle wasting and, again, the distribution of weakness. The weakness in the lower limbs is preferentially for hip flexion, foot extension, and for flexion at the knee. The tendon reflexes are increased and the plantar response may be extensor - the toes extend and fan when the sole of the foot is scraped.

Characteristic Gait:

The gait cannot be high stepping because of hip flexion weakness, but weakness of foot extension will tend to cause the patient to catch the toe on the ground when walking and may cause trips and falls. The solution is for the patient to swing the whole lower limb sideways in a circular movement when walking so as to clear the toes (circumducting gait)

Deafferentation:

The Anatomy:

Receptors in the feet and toes signal the position of the limb in space (proprioception). Lack of feedback from the lower limbs when walking drastically alters the automatic control of ambulation, which in large measure is a reflex function. Without input there can be no reflex output. Severe loss of proprioception can be as functionally devastating as paralysis.

Sensory receptors in the joints feed back through the nerves to the nerve roots. The cells of these sensory nerves lie outside of the spinal cord, but within the spinal canal and are situated in the dorsal root (dorsal root ganglia). Electrical impulses are relayed from the periphery into the spinal cord where the various sensory nerve fibers split into different ascending sensory tracts, depending on the function they subserve. Sensation for pain and temperature is carried in fibers which cross to the opposite side of the cord through its center, and then ascend to the thalamus as the spinothalamic tract. Sensation for proprioception does not cross low down in the cord, as does sensation for pain, but ascends immediately in the back or posterior part of the spinal cord on each side as the "dorsal columns." These tracts cross at the very top of the spinal cord and also synapse (connect with the next nerve in the chain) in the thalamus which is a way station on the way to the cortex.

The Examination:

The neurologist tests proprioception by asking the patient, with eyes closed, to identify the position of the big toe, which is passively either flexed or extended. The patient should, normally, be able to identify even very subtle up and down movements of the toes. Loss of position sense is usually due to pathology in the dorsal columns at any level, but in patients with a very severe neuropathy affecting the nerves in the legs, the large rapidly conducting peripheral nerve fibers can be compromised which disturbs proprioception.

Characteristic Gait:

In patients with proprioceptive loss the gait is very slightly high stepping and the foot strikes the ground fairly forcefully at the heel. The front part of the foot then slaps down on the ground. Some texts refer to this as a stamping gait. The Romberg test will be positive: one asks the patient to stand upright with the feet together with eyes closed. Normally, reflex activity will keep the subject upright and steady. If there is lack of proprioception the patient sways alarmingly and may even fall. In these patients vision compensates for poor proprioception.

Cerebellar ataxia:

The Anatomy:

The cerebellum receives input from the lower limbs, integrates it, and sends it on to the brainstem nuclei and higher centers. The cerebellar hemispheres are responsible for coordination of limb movement, and the midline cerebellum (vermis) coordinates trunk movement. The phylogenetically oldest part of the cerebellum (floccular nodular lobe) is strongly connected to the central and peripheral balance (vestibular) regions and acute dysfunction here can cause vertigo and twitchy movements of the eyes (nystagmus), which is discussed in the next section.

Dysfunction of the cerebellum or its connections results in ataxia or incoordination. Movements are jerky and broken up into their component parts.

The Examination:

The neurologist tests for cerebellar function in the upper limbs by asking the patient to touch an upheld examiner's finger and then his/hernose, back and forth. Patients with cerebellar ataxia perform the test in a jerky uncoordinated fashion and often miss and overshoot the targets. When testing the lower limbs the patient is asked to run the heel of one leg up and down the shin of the other in a smooth fashion. If the movement is jerky and the heel sways off the shin repeatedly, cerebellar dysfunction is diagnosed. The inability to stand or sit steadily, even if the limbs are normal implies vermis dysfunction.

Characteristic Gait:

The ataxic gait is characterized by a wide base to aid balance, and reeling, uncoordinated steps, much as one might see in an intoxicated individual.

Dizziness:

The Anatomy:

Vestibular reflexes originate in the balance organs of the inner ear and allow for normal gait and posture. A sensation of spinning is called rotary vertigo and is usually secondary to inner ear dysfunction. The semicircular canals are sensitive to motion and a sac called the utricle is sensitive to the pull of gravity. Dizziness arising from dysfunction in these structures is often labeled a "vestibulopathy."

The patient complains of a spinning sensation- either the world seems to be spinning or the patient has a sensation of head spinning. The symptoms are aggravated by head movement and associated with pallor, sweating, nausea, and vomiting. When the problem is more chronic, there may be some mild to moderate sensation of spinning, but there is also a feeling of imbalance, which is accompanied by veering toward the affected side when walking.

The most important sign to support the diagnosis of vestibulopathy is nystagmus: The patient is asked to visually track the examiners finger which is held to one or other side. On gaze laterally the eyes jerk or twitch. There is a slow deviation to one side and then a rapid twitch to the other side. The slow part of nystagmus is the pathological part and the quick phase is corrective. This kind of nystagmus is called "jerk, " "phasic, " or "gaze evoked" nystagmus.

Because the imbalance draws the patient to one side, if the patient is asked to stamp in place with the eyes closed, he may unconsciously turn toward the affected side. (Unterberger's test)

The physician must determine if the vertigo is because of primary dysfunction in the inner ear, or in the nerve supplying the inner ear (vestibular nerve), or in the central connections of the vestibular nerve in the brain stem. Probably the most sensitive divider between central and peripheral vestibulopathy is the "company" that the vertigo keeps - if other stem or tract signs are evident it's a central problem. The character of the nystagmus may also help.

Characteristic Gait:

Sometimes the patient complains only of a mild feeling of imbalance or dysequilibrium without frank rotary vertigo. The examination is largely negative, but the patient may sway towards the abnormal side. In more severe cases there is falling towards the abnormal side.

Extra-pyramidal disorders:

The Anatomy:

Extra-pyramidal (i.e. not pyramidal) disorders are characterized by problems with the basal ganglia, as opposed to the major motor descending tract called the "pyramidal tract"; hence the nomenclature "extra" pyramidal. Dysfunction in the basal ganglia usually results in a paucity of movement (hypokinetic disorders) of which Parkinson's disease is the prototype. Occasionally there are additional unwanted movements (hyperkinetic disorders) as in Huntington's chorea.

The circuitry and connections of the nuclear masses in the basal ganglia region are complex: The striatum is made up of the caudate nucleus and the putamen. Also included in the deep nuclear masses are the globus pallidus, substantia nigra, subthalamic nucleus, and the thalamus. The basal ganglia project to the cortex via the thalamus and facilitate smooth cortico-spinal function.

Parkinson's disease:

The essential deficit in Parkinson's disease is a deficiency of a neurotransmitter (a chemical that allows cells to synaptically stimulate each other) called dopamine (DOPA). This is manufactured mainly in a region called the substantia nigra, seen as a blackish stripe at the base of the midbrain. The substantia nigra is darkly colored because the cells contain neuromelanin, a black pigment; in the brains of patients who have died of Parkinson's disease the area is pale due to a of lack of these cells. Degeneration of the substantia nigra in Parkinson's disease causes DOPA deficiency. Normally the dopamine made in the substantia nigra is carried to the striatum where it activates receptor neurons and drives the system. Lack of dopamine results in lack of movement or hypokinesia. The reverse, excessive DOPA, causes excess movement.

Characteristic Signs and Gait:

The three cardinal signs of Parkinson's disease are hypokinesia or lack of movement, rigidity or increased tone, and tremor. The hypokinesia is manifest as a lack of spontaneous fidgety movements lack of facial expression (mask-like face), or decreased arm swing when walking. Tone is increased most in the proximal muscles (those closest to the center of the body) but also in the peripheral muscles, which cannot be easily passively moved by the examiner. If there is a superimposed tremor a sensation of cogwheeling or ratcheting is felt when the wrist is passively rotated. The tremor, when present, is often called "pill rolling" with fairly rapid to and fro movement of the index finger on the thumb.

The gait is narrow based. Steps are small. The patient is easily pushed backward and may even fall backward spontaneously (retropulsion). Gait initiation is defective and it's hard to get started - the patient may take a few hesitant, preliminary steps. The body becomes flexed, the arms don't swing when walking, and may spontaneously flex at the elbows. Curiously, the steps become quicker and quicker (festinating or hurrying gait) as walking progresses.

Patients with Parkinson's disease treated with excessive doses of dopamine may become hyperkinetic, with uncontrollable, often somewhat twisting movement of the limbs, and sometimes even of the neck and facial muscles (DOPA dyskinesia).

Hyperkinetic disorders:

Sudden twitch like movements, seemingly fragments of normal movement but in isolation, are called chorea. Huntington's disease is an example of a genetically determined form of chorea. Slower, more writhing and serpentine or sinuous movements with momentary maintenance of an abnormal posture are called athetosis.

These disorders will only very rarely present as a gait disorder.

Frontal lobe disorders:

The PAnatomy:

The frontal lobe is the highest center for control of walking. It receives information from lower centers and in turn is capable of taking over full control of gait. The very highest center of bladder control is frontal and in frontal lobe disorders there may be incontinence. Disorders of the frontal lobes are suspected in the presence of characteristic gait and bladder disorders, but also if there are cognitive changes. These may manifest as a personality change, slowness of thought or action (abulia), or even the reverse, with senseless joking and punning.

The pathology may be degeneration of the frontal lobes which is largely untreatable, but treatable causes include frontal brain tumors and hydrocephalus. The ventricles are spaces filled with water (cerebrospinal fluid - CSF) deep within the brain and if the ventricles enlarge they do so at the expense of normal brain tissue. Enlargement in the frontal area interferes with function. The CSF is continually pumped into the ventricular system and circulates through a sort of plumbing system to be reabsorbed outside the brain. An obstruction to this flow inside the brain causes the ventricles to enlarge proximal to the obstruction. (obstructive hydrocephalus). Diminished absorption outside the brain causes diffuse ventricular enlargement (communicating hydrocephalus). An obstruction in the plumbing system causes increased pressure which can be intermittent, but the blockage can be surgically bypassed or shunted with resultant improvement in ventricular size and of the frontal signs. Sometimes the cause of the obstruction can be surgically removed.

Pathology such as trauma with bleeding, or meningitis may block the pathways outside of the brain, resulting in large ventricles without a central obstruction. The intraventricular pressure must be high initially to cause the ventricles to enlarge, but once hydrocephalus is established the size of the ventricles is maintained even at normal pressures leading to the term "normal pressure hydrocephalus" (NPH). This pressure/volume relationship obeys Pascal's law about pressures in a sphere.

The Examination:

Patients with frontal dysfunction may repeat the same words or actions over and over again (perseveration) and they lack flexibility of thought and action so that they stay on one track and cannot copy a series of different hand postures. Certain reflexes help the clinician to diagnose a frontal disorder: the patient may involuntarily grasp the examiner's hand or fingers (grasp reflex), and scraping the palm results in puckering of the chin (palmo-mental reflex). They may have memerory disturbances and personality changes.

Characteristic Gaits:

Various types of gait disorders are produced by frontal lobe dysfunction

Ignition failure: The inability to get started. The patient takes a few hesitant steps on the spot when attempting to initiate ambulation. Once this initial difficulty has passed the gait is normal.

Classical frontal gait disorder: Ignition failure as above, but thereafter the gait is narrow based, with small steps and frequent stops and starts.

Frontal ataxia: The gait is bizarre and incoordinated. The explanation for this seemingly cerebellar-like syndrome is the strong influence exerted by the frontal lobes on the cerebellum by a tract called the "fronto-ponto-cerebellar tract" which describes exactly where it goes; disordered frontal control leads to disordered cerebellar function.

Lower Half Parkinsonism: The gait is as described as in classical frontal gait disorder, but the arms are not affected; the legs don't work normally, but the arms pump furiously. White matter disease secondary to microvascular disease in the frontal lobe is the explanation.

NPH can be shunted with resolution of the frontal signs, but it is hard to prove the diagnosis of hydrocephalus because the ventricles also enlarge in cases of brain atrophy. The workup is designed to distinguish atrophy (hydrocephalus ex vacuo) from NPH. No one would want to operate without being able to offer the patient a reasonable expectation of success. Over the years various confirmatory tests have been tried and many have failed. Currently, improvement of gait after draining a large volume spinal fluid via spinal tap (lumbar puncture) is suggestive. One can also study pressure dynamics - sterile saline is injected in small aliquots through a spinal needle into the spinal subarachnoid space and the pressure is measured after each injection. Normally the system can absorb fairly large amounts of fluid, normal compliance. A precipitous rise in pressure well above what would be expected suggests abnormal compliance and is predictive of a good result with shunting.

Psychogenic gait disorder:

At times non-organic factors result in gait dysfunction. The clues are:

Normal neurological examination

Momentary fluctuations of stance and gait, often in response to suggestion.

Uneconomic postures with wastage of muscular energy

Sudden buckling at the knees, usually without falls

Excessive slowness or hesitation of locomotion incompatible with neurological disease

The Examination:

While the astute clinician is usually fairly certain that the disorder is Functional and not organically based, these patients require extensive workup to be absolutely certain of the diagnosis. The concern is for possibly missing treatable pathology which happens to look functional or psychiatric. When the characteristics of the gait disorder suggest a psychogenic cause, imaging is normal then a psychiatric consultation is called.

The term "walking on ice" describes one kind of cautious and functional gait disorder. In other patients, the gait is called "astasia-abasia, " coined by Jaccoud more than a century ago. The patient, on a narrow base, sways wildly in all directions with flailing arms and excessive trunk sway, and looks to be about to fall, but never does. In severe phobic gait disorders the patient will cautiously walk around the room holding on to the walls. Steps are slow and deliberate -the "cautious gait."

Next steps: The examination of the patient diagnoses the site of the pathology. It remains to define exctly what that pathology is. To this end the neurologist will decide what further studies are necessary to complete the diagnostic workup. This generally begins with a series of blood studies and imaging. Nowadays the imaging modality of choice is magnetic resonance imaging which is highly sensitive and is non-invasive.

This review has been designed to afford a basic understanding of the physiology and pathophysiology of walking. The pathology is very variable and dictates management as decided by the neurologist. Only when the pathology has been elucidated can a plan of management be formulated and this will be individualized for any particular patient.

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Normal MRI of Brain with Normal ventricles

BASAL GANGLIA

HYDROCEPHALUS