Robert Wartenberg - neurologic examination
Robert Wartenberg - exame neurológico
Robert Wartenberg was born in 1887 in Grodno, Belarus, then part of the Russian Empire[1 ]. He received his medical degree from the University of Rostock, Germany, in 1919,
and was, for many years, associated with the University of Freiburg, where he became
Professor of Neurology in 1933[2 ]. With the Nazi regime in power, rising anti-Semitism led him to flee Germany in
1935. After relocating to the United States in 1936, he re-engaged in his neurology
career at the University of California Medical School in San Francisco, where he was
appointed Clinical Professor of Neurology in 1952[2 ].
Wartenberg was an internationally recognized neurologist, earning an honorary membership
in several foreign societies. Of note, in 1953, the California Medicine Journal[3 ] published the following announcement: “Dr. Robert Warten
berg, clinical profe
ssor of neurology, U
niversity of Califor
nia Hospital, has be
en elected a corresp
onding member of the
Rio de Janeiro Soci
ety of Neurology”.
Wartenberg’s academic accomplishments were vast. He believed in a “sacred obligation”
to his students, and reportedly his lectures were unforgettable events[1 ]. Wartenberg made over 150 scientific contributions, including four books[1 ]: T
he Examinati
on
of Reflexes: A Simpl
ification (1945)[4 ]; Hemifaci
al Spasm (1952)[5 ]; Diagnosti
c Tests in Neurology (1953)[6 ]; and Neuritis, Sensory Neuritis, Neura
lgia (1958)[7 ].
He was reputed to be one of the foremost semiologists of his time. He strived to abolish
unnecessary eponym designations, leading an effort to replace them with designations
that were descriptive of the underlying pathophysiology[8 ]. In fact, he was known to be very critical of the neurological literature, somewhat
intolerant of carelessness, albeit with a constructive intent.
We pay homage to Wartenberg’s tradition of simplifying the examination by briefly
discussing five of his seminal neurological signs.
TENDON PALPATION TEST
A lesion of the lower motor neurons lead to muscle hypotonia, resulting in tendon
slackness. This is best seen in the Achilles tendon. With the patient standing upright,
weight equally distributed onto both legs, the examiner gently grasps the patient’s
ankles, placing his thumbs directly over the Achilles tendons. Pressure is gradually
exerted over each tendon, while comparing the resistance offered against the thumbs
([Figure 1 ]).
Figure 1 Tendon palpation test.
In a normal person standing flat onto his feet, the Achilles tendon has a hard consistency.
In unilateral lesions of the sciatic nerve the Achilles tendon has a softer consistency
when compared to the normal side.
This sensitive test may indicate the presence of a lower motor neuropathy at a very
early stage when no evidence of muscle wasting, weakness, or even diminished ankle
jerk is present. A soft Achilles tendon may thus be an early sign of sciatic neuropathy.
When positive, this test corroborates an organic peripheral lesion of the nervous
system, but a negative test cannot exclude it[6 ].
LID VIBRATION TEST
The seemingly smooth process of sustained voluntary muscle contraction is a result
of the continuous integration of multiple underlying discrete and successive contractions.
This fine-tuning mechanism is evident in the orbicularis oculi as a palpable vibratory
sensation that declines with weakness. It can be felt by applying gentle lateral traction
at the outer canthus while the patient maintains forceful eyelid closure ([Figure 2 ]).
Figure 2 Method of lid vibration test.
Diminished lid vibration is a very sensitive sign, occurring early in cases of slowly
evolving facial palsy. Conversely, its return to normality occurs slowly and late
in the process of recovery. In fact, it may remain diminished as a sole indication
of an old facial palsy. As such, diminished lid vibration may be the first, as well
as last, sign detected in the natural history of a facial palsy. Despite its sensitivity,
it is not specific in distinguishing central from peripheral facial lesions, being
present in both[6 ].
ASSOCIATED MOVEMENT OF THE THUMB
ASSOCIATED MOVEMENT OF THE THUMB
Volitional hand movements require precise control of agonist, antagonist, and synergist
muscles. This orchestration is compromised by lesions of central descending motor
pathways, resulting in unusual patterns of motor activation. One such pattern is observed
in the spastic paretic hand as an associated movement of the thumb.
The patient is asked to pull his four fingers, flexed at the terminal phalanges, against
resistance offered by the examiner’s similarly flexed fingers ([Figure 3 ]).
Figure 3 Associated movement of the thumb. In mild spastic paresis the thumb moves toward
the palm. The examiner is wearing a wristwatch.
In a normal person, the thumb remains extended and abducted. Conversely, spastic paresis
of the hand results in involuntary thumb adduction, flexion, and opposition. This
constitutes a very early sign, and may be seen in incipient spastic hand paresis[6 ].
WRIST DROP TEST
Weakness of wrist extension results in a hand droop when the patient’s pronated forearm
is held horizontally, and fingers are relaxed. Inspection alone cannot differentiate
if this phenomenon is due to a central or peripheral lesion. However, clenching the
fingers while the hand is in this position can make this distinction[6 ] ([Figure 4 ]). Normally, flexion of the fingers is accompanied by extension at the wrist as an
associated movement. This motor response is preserved with lesions affecting central
motor pathways, and is lost with peripheral lesions.
Figure 4 Wrist drop (A). In flaccid paresis wrist flexion is exacerbated (B). In spastic paresis
involuntary wrist extension occurs (C).
The patient is asked to grasp an object with his affected hand. With peripheral lesions
affecting the extensor musculature, such as a radial neuropathy, dorsiflexion is absent.
In fact, wrist flexion may be accentuated by increasing effort to tighten the grip.
With central lesions, wrist dorsiflexion occurs involuntarily.
ACCESSORY NERVE TEST
The spinal accessory nerve innervates the upper trapezius muscle, which acts to elevate
the shoulder. This thin nerve lies superficially and is easily traumatized, often
an iatrogenic lesion of the posterior triangle of the neck[9 ].
In the event of an accessory nerve lesion a shoulder droop occurs. This displacement
results in an apparent length discrepancy of the upper limbs. The patient is examined
upright with arms hanging loosely at the sides. The level at which the fingertips
touch the thighs are compared. On the affected side the fingertips touch the thigh
at a lower level than on the healthy side ([Figure 5 ]).
Figure 5 Accessory nerve test. Fingertips on affected side (right) extend below the level
on healthy side (black line).
Robert Wartenberg was a respected figure in the global neurological community, in
great measure due to his didactic acumen[2 ]. In today’s overly technological environment, remembering Wartenberg’s signs may
rekindle the art of examination.
