Senile Gait: Correlation with Computed Tomographic Scans William C . Koller, M D , PhD,* Robert S. Wilson, PhD,: Sander L. Glatt, MD,S Michael S. Huckman, MD,B and Jacob H . Fox, MDS

Gait difficulties unrelated to clinically obvious neurological or systemic diseases but associated with aging are referred to as senile gait [Z]. Degeneration of the frontal lobes, basal gan- glia, o r cerebellum as well as hydrocephalus have been pro- posed as possible anatomical causes [ I , 3, 43.

We evaluated computed tomographic (CT) scans in 16 pa- tients (10 men, 6 women; mean age, ' 5 . 3 years) with senile gait disorder. Senile gait was defined as the gradual appear- ance of a broad-based gait with small steps associated with diminished arm swing, stooped posture, flexion of the hips and knees, uncertainty and stiffness in turning, occasional difficulty initiating steps, o r a tendency toward falling 121 occurring without a clear etiology in individuals over age 60. Eight patients were symptomatic; 0 were demented. The con- trol population consisted of 59 patients (28 men, 2 I women; mean age, 72.6 years) with normal gaits who complained of cognitive loss or were healthy participants in a longitudinal study of aging. Patients with a history of cerebrovascular dis- ease, neurological disorders, chronic alcoholism, orthopedic or joint disease, diabetes mellitus, or other serious medical disease were excluded. T h e diagnosis of dementia was based on a history of progressive intellectual decline with absence of focal neurological lesions o r systemic or psychiatric disease and by psychometric testing. All patients received C T scans which were analyzed blindly by a radiologist for supratento- rial and infratentorial atrophy using methods previously de- scribed [ 5 , 61. Data analysis was accomplished by Student t- test and analysis of variance.

The 16 patients had the following abnormalities: inability to pcrform tandem gait (16 patients), wide-based gait (14), poor truncal stability (1 2 ) , gait dysrhythmia (1 1 ), flexed at- titude (101, shortened steps ( lo ) , bradykinesia (8) , loss of associated arm movement ( 5 1, diminished ability to advance steps t 4 ) , gait apraxia (2), and narrow base (1). Patients did not differ from controls in infratentorial CT measures except for a significantly increased fourth ventricle ratio ( p <: 0.05). The only significant difference in supratentorial measures (Table) was dilatation of the lateral and third ventricle with- out changes in cerebral atrophy ( p < 0.01).

T h e clinical picture of senile gait is variable and imprecisely defined. It is stated that the inability to walk tandem is univer- sal in the very old 141. Potvin and associates [ 8 ] , however, concluded that tandem gait is unaltered by age. Prakash and Stern 191 reported that a broad-based gait was often present in their elderly patients. Senile gait is said to be difficult to distinguish from parkinsonism at times [ 4 ] . Our patients dis- played wide-based gaits and inability to tandem walk, associ- ated with a flexed posture. It is unclear whether multiple types of senile gait or a single progressive disorder exists. Senile gait occurred with equal frequency in nondemented and demented patients.

Mean Vafnes of Supvatentoviai Compated Tomographic Measuvenients in XGKVZUI and Abnormal Gait Patientc

~~

Normal Gait Abnormal Gait

Variable Normal Demented Normal Demented 7 No. of patients 28 31 9

Age 72.6 71.6 74.9 75.7 Hifrontal ratio 0.31 0.37 0.38 0.42 Bicaudate ratio 0.14 0.18 0.17 0.22 Third ventricle 0.04 0.05 0.06 0.07

ratio

atrophy score Cerebral sulci 1.75 1.87 2.29 2.13

Few facts illuminate the anatomical basis of senile gait. Critchley [21 suggested that the gait of the elderly was a manifestation of extrapyramidal dysfunction. Disease of the mesial frontal lobes produces a gait disorder referred to as apraxia of gait [77. Alternatively, senile gait has been attrib- uted to cerebellar dysfunction [4] . Degeneration of the cere- bellar vermis results in a gait disorder characterized by a wide-based stance, inability to perform tandem walking, and truncal instability, characteristics similar to the predominant signs observed in our senile gait patients. However, we found no CT evidence of atrophy of the vermis o r enlargement of the superior cerebellar cistern.

Sensory abnormalities have been suggested as responsible for gait and postural difficulties 141. A d a m and Victor specu- late thar the peculiar gait of the aged is due to a combined frontal lobe basal ganglia degeneration [ 11. Fisher has sug- gested that senile gait is caused by hydrocephalus and that the instability could be reversed by cerebrospinal fluid shunting 131. In the present investigation ventriculomegaly, particu- larly at the level of the frontal horns of the lateral ventricles and the caudate nucleus, unassociated with increased cerebral atrophy, correlated with the presence of senile gait abnor- malities. Few patients met the clinical o r radiological criteria for normal pressure hydrocephalus. Only one had urinary incontinence, and most had prominent corticosulcal enlarge- ment. Thus the CT scan appearance is different from that reported by Fisher 131. W e do not advocate cerebrospinal fluid shunting for senile gait patients.

Supported in part by Grant AGO0905 from the US Public Health Service

Presenred in part at the 107th Annual Meeting of the American Neurological Association, Washingron, DC, Sept 30-Oct 2, 1982

Department o/ $Neurology and f Psychologt

Rush Medical College Chicago. IL 60612 'Department of Neuvolog Unwersitj n/ Illinon College o/ Medzctne Chicago. 1L 60612

and 9 Department of RadzoloRy

Notes and Letters 343

References 1. Adams RD, Victor M: Principles of Neurology. New York,

2. Critchley M: Senile disorders ofgait. Geriatrics 1:364-370, 1948 3. Fisher CM The role of hydrocephalus in unexplained late life gait

disorders. Ann Neurol 89-92 , 1980 4. Greenhouse AH: Neurologic disability in normal aging. In Joynt

RJ (ed): Seminars in Neurology. New York, Thieme-Stratton,

5 . Huckman MS, Fox J, Topel J: The validity of criteria for the evaluation of cerebral atrophy by computed tomography. Raiiiol- oev 11645-92. 1978

McGraw-Hill, 1977, p 405

1981, pp 13-21

6. K o k r WC, Perlik S, Glatt S, Huckman MS. Fox JH: Cerebellar atrophy demonstrated by computed tomography. Neurology

7. Mcyer J, Barrow D: Apraxia of gait: a clinico-physiological study. Brain 83.761-784, 1960

8. Potvin AR, Syndulko K, Tourtellotte WW, Lemmon JA, Porvin JH: Human neurologic functions and the aging process. J Am Geriatr Soc 28: 1-9, 1980

9. Prakash C, Stern C: Neurological signs in the elderly. Age Ageing 2:24-27, 1973

(NY) 31:405-412, 1981

“Salt and Pepper on the Face” Pain in Acute Brainstem Ischemia L. Caplan, MD, and P. Gorelick, M D

Pain or dysesthesias are uncommon in acute brain ischemia. Numbness or tingling and prickling feelings are frequent complaints in acute lesions of the medial lemniscus, ven- trolateral thalamus, parietal white matter, and somatosen- sory cortex, but pain, when it occurs in ischemic lesions of these structures, usually develops weeks or months later [6]. The lateral medullary syndrome provides an exception to this rule because patients often note sharp, jabbing, or burning pain in the ipsilateral eye or face at the onset of their stroke. Pain in the lateral medullary syndrome is probably related to involvement of sensory neurons in the nucleus of the descending tract of V [ 3 , 51, a rostral exten- sion of the substantia gelatinosa of the spinal cord [ 11. We call attention to three patients with a curious variety of fa- cial pain as a prominent and acute symptom in lesions clini- cally attributable to ischemia of medial brainstem struc- tures.

The first patient, a hypertensive 54-year-old man, was surprised at work by a peculiar and shocking sensation in his face. It felt “as if salt and pepper had been thrown in my eyes and face.” The feeling was more pronounced on the right side of his face and was accompanied by slight dizzi- ness, lasted seconds to a few minutes, and recurred on five separate occasions during the day. During the last episode he noticed that his left limbs were weak. Examination re- vealed a “pure motor hemiparesis” sparing the face and difficulty sustaining right conjugate gaze. The electroen- cephalogram was normal. The sensory experience was transient. The unpleasant feeling was gone by the next day but the hemiplegia persisted.

A 40-year-old hypertensive diabetic woman developed pain in the right eye and behind the right ear while bowling one evening. She awakened the next morning with dizzi- ness and pain in the right eye, slurred speech, a “drunken” gait, and weakness of the left leg. “It felt as if pepper had been poured into the eye.” There was transient numbness around the left lip. Examination revealed a left hemiparesis with exaggerated left deep tendon reflexes and a left Babinski sign. There was no tingling or objective sensory change. The unpleasant facial sensation was temporary. Lumbar puncture, plain and enhanced CT computerized tomographic scans, and carotid and vertebral angiography were normal.

A 58-year-old man (Case 8 in [2]) had transient vertigo and left limb paresthesias. A month later, he developed a left hemiplegia accompanied by a persisting and severe burning pain in the face that was bilateral but more severe in the left eye and the nose. There was a metallic taste in his mouth. Angiography revealed a midbasilar artery occlu- sion.

All three patients had ischemic lesions clinically localized to the brainstem. In the first, dizziness, gaze paresis to the ipsilateral side, and crossed facial sensory and limb motor findings led us to conclude that the hemiplegia was due to a lacune in the paramedian pontine base. In the second pa- tient, dizziness, crossed facial sensory and limb motor ab- normalities, and normal computerized tomogram favored a brainstem lesion. The history of hypertension and diabetes and normal arteriography favored a lacunar cause of the stroke. Transient tegmental ischemia may accompany brainstem lacunes. The third patient had a documented basilar artery occlusion, and clinical dysfunction was lim- ited to paramedian structures (no nystagmus and no cere- bellar or spinothalamic tract signs).

The experience of “salt and pepper on the face” burning pain is novel; we could find no mention of it in prior re- ports. Fisher 141 mentions one patient with trigerninal pain “of the type seen in lateral medullary infarction” in his ex- perience with basilar artery obstruction. The paramedian location of the other signs, absence of the usual accom- paniments of the lateral medullary or pontine syndromes, and bilaterality would be evidence against the pain originating in the laterally placed descending tract of V, the nucleus of the descending tract of V, or the principal sen- sory nucleus of V (which is more rostral but also laterally placed). Fibers from the descending tract of V synapse at the nucleus of the descending tract of V and then cross to append themselves to the medial aspect of the contralateral spinothalamic tract. The exact location of the decussation of these quintothalamic pain fibers is unknown but is surely paramedian, and involvement of these fibers could explain the bilaterality and painful character of the sensation. This hypothesis must remain purely speculative without post- mortem documentation of the infarctions and more anatomical study of the course of the quintothalamic fibers. We call attention to this curious facial sensory experience as a clue to ischemia in the paramedian brainstem.

Department of Neurology Michael Reese Hospital 29th 6 Ellis .floe Chirwgo, IL 6061 6

344 Annals of Neurology Vol 1 3 N o 3 March 1083