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Rare Clinical Image of Kennedy’s Syndrome
Sir,
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Bulbar motor neuron disease, often referred to as bulbar
palsy or bulbar onset motor neuron disease, is a subtype of
motor neuron disease (MND) that primarily affects the motor
neurons located in the bulbar region of the brainstem.[1] This
nYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8K2+Ya6H515kE= on 05/02/2024
condition is characterized by the progressive degeneration
of these motor neurons, leading to impairments in speech,
swallowing, and sometimes breathing.[2] It falls under the
broader category of neurodegenerative disorders, sharing
similarities with conditions like amyotrophic lateral
sclerosis (ALS). [3] The bulbar region of the brainstem is
crucial for controlling essential functions such as chewing,
swallowing, speaking, and breathing. Motor neurons in
this area transmit signals from the brain to the muscles
responsible for these actions. However, in bulbar motor
neuron disease, these neurons gradually degenerate and lose
their ability to function properly, resulting in the hallmark
symptoms associated with the condition. One of the earliest
and most prominent symptoms of bulbar motor neuron
disease is dysarthria, a speech disorder characterized by
slurred or unintelligible speech.[4] In addition to speech and
swallowing impairments, individuals with bulbar motor
neuron disease may also experience weakness and wasting of
the facial muscles, leading to facial drooping or difficulty with
facial expressions. The exact cause of bulbar motor neuron
disease remains unclear, although it is believed to involve a
combination of genetic, environmental, and lifestyle factors.
Like other forms of motor neuron disease, bulbar onset
disease is characterized by the progressive degeneration of
motor neurons, leading to muscle weakness and eventual
paralysis.[5]
An 85‑year‑old male patient visited the neurology OPD with
complaints of left‑side weakness, difficulty swallowing solid
food, mild discomfort with liquid food, and difficulty in speech
articulation. He had a 15‑year history of hypertension and had
recently stopped taking antihypertensive medications. Over
a b
Figure 1: MRI brain showing (a) Susceptibility weighted imaging with right subdural
bleed, (b) T1WI imaging showing Subacute bleed
460
several months, his symptoms had progressively worsened,
including slurred speech, recurrent choking during meals,
and weakness in his facial muscles. The initial examination
showed the patient to be conscious, cooperative, and well
oriented. He was examined in a specific position, and his
Glasgow Coma Scale score was E4V1M6. Additionally, the
examination revealed the loss of certain reflexes, such as the
gag reflex and jaw jerk reflex. Sensory examination indicated
intact sensations, while motor examination showed reduced
strength in the left upper and lower limbs. Diagnostic tests,
including an MRI scan and blood tests, confirmed a diagnosis
of bulbar disease. Figure 1a and b reveal the presence of a
well‑defined extra‑axial crescent‑shaped collection on the
right cerebral hemisphere, with a maximum thickness of
2.5 cm. This collection appears hyperintense in T1WI and
hypointense in T2/FLAIR, consistent with an early subacute
subdural hematoma. The mass effect is evident, causing
effacement of sulcal spaces and the ipsilateral lateral ventricle,
along with a midline shift of 6 mm to the left. Additionally,
there is focal right frontal periventricular white matter
edema. Age‑related changes are observed, with prominence
in sulcogyral spaces, the cerebellar folia, and the ventricular
system.
Patient’s consent
The patient’s guardian has provided a comprehensive and
thorough consent. The patient’s identity has been effectively
anonymized. The journal will not assume responsibility for any
legal or medical issues that may arise from concerns regarding
the patient’s identity or any other matters associated with the
public dissemination of the article.
Ethical statement
This study was conducted in adherence to the ethical principles
outlined in the World Medical Association Declaration
of Helsinki. According to local guidelines pertaining to
single‑patient reports, Institutional Review Board approval was
not deemed necessary. The patient provided written, informed
consent for the publication of both data and images, and this
consent was formally documented through their signature.
Patient consent declaration
The authors affirm that they have obtained all necessary patient
consent forms. Within these forms, the patient(s) has/have
granted consent for the publication of their images and other
clinical information in the journal. The patients are aware that
their names and initials will not be disclosed, and diligent
measures will be taken to protect their identity. However,
complete anonymity cannot be assured.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
© 2024 Neurology India, Neurological Society of India | Published by Wolters Kluwer - Medknow
 Neuroimage

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tweak, and build upon the work non‑commercially, as long as appropriate credit is given and
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Rajas P. Mudey, Sharath Hullumani V

Department of Paediatric Physiotherapy, Ravi Nair
Physiotherapy College, Datta Meghe Institute of Higher
Education and Research, Wardha, Maharashtra, India

Address for correspondence:
Rajas P. Mudey,
Department of Paediatric Physiotherapy, Ravi Nair Physiotherapy
College, Datta Meghe Institute of Higher Education and Research,
Wardha, Maharashtra, India.
E‑mail: rajasmudey123@gmail.com
How to cite this article: Mudey RP, Hullumani VS. Rare Clinical Image
of Kennedy’s Syndrome. Neurol India 2024;72:460-1.
Submitted: 29‑Feb‑2024 Revised: 28‑Mar‑2024
Accepted: 28‑Mar‑2024 Published: 30-Apr-2024
© 2024 Neurology India, Neurological Society of India | Published by Wolters Kluwer - Medknow

Neurology India | Volume 72 | Issue 2 | March-April 2024 461