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Horner’s syndrome due to Pancoast tumour

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Horner’s syndrome due to Pancoast tumour

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INTRODUCTION
A 37-year-old male, a life-long non-smoker,
presented to medicine out-patient service with
pain in the right shoulder and upper chest
radiating to right upper limb for the past one
year. He also complained of cough with scanty
mucoid sputum for the past two weeks. General
physical ex aminatio n re veale d findings
suggestive of Horner’s syndrome (Figure 1A).
On respiratory system examination, findings
suggestive of a right upper lobe mass lesion
were evident. Chest radiograph (Figure 1B)
showed a rig ht upper lobe mass lesion.
Computed tomography (CT) of the chest
(Figure 1C) revealed an irregular lobulated soft
tissue density mass lesion in the apex of the
right lung (Pancoast tumour) and destruction
Special Feature:
Horner’s syndrome due to Pancoast tumour
J. Harikrishna,1 B. Raga Deepthi,1 V. Arun Raja,1 P. Suneetha,1
Amit Kumar Chowhan,2 B. Vijaya Lakshmi Devi,3 Abha Chandra,4 Alladi Mohan1
Departments of 1Medicine, 2Pathology, 3Radiodiagnosis, 4Cardiothoracic Surgery,
Sri Venkateswara Institute of Medical Sciences, Tirupati
Harikrishna J, Raga Deepthi B, Arun Raja V, Suneetha P, Chowhan AK, Vijaya Lakshmi Devi B, Abha Chandra, Mohan A.
Hor ne r ’s synd rome due to Pancoast tumo ur. J C lin Sc i Res 2014 ;3 :150-2. DOI: ht tp:/ /d x. do i. org/10. 153 80/2277-
5706.JCSR.13.051.
of the first rib. CT-guided tru-cut biopsy from
the lesio n co nfirme d the diagno sis o f
adenocarcinoma of lung (Figure 1D).
Horner’s syndrome results from the interruption
of the oculo-sympathetic nerve supply between
its origin in the hypothalamus and the eye. The
first-order neurons arise from the hypothalamus
and synapse at Budge’s centre in spinal cord
(C-8 to T-2 level). Second-order neurons exit
the spinal cord at the T-1 level and travel close
to the apex of the lung and synapse at the
superior cervical ganglion. Third-order neurons
travel along with the internal carotid artery
Corresponding author: Dr Alladi Mohan,
Pr ofess or a n d Hea d , Depa rtment of
Medi ci ne, Sri Venkateswara Institut e of
Medical Sciences, Tirupati, India. e-mail:
alladimohan@svims.gov.in
Received: 08 September, 2013.
Figure 1(A): Clinical photograph showing right-sided
ptosis, miosis and apparent enophthalmos suggestive of
Horner’s syndrome
Figure 1(B): Chest radiograph (postero-anterior view)
showing a dense opacity in the right upper zone
suggestive of a mass lesion with destruction of the
anterior and lateral end of first rib (arrow)
Horner’s syndrome due to Pancoast tumour Hari Krishna et al
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DOI: http://dx.doi.org/10.153 80/2 277 -5706.JCSR.13 .05 1
151
through the cavernous sinus and enter the orbit
wit h t he thir d cranial ner v e. 1 Horner ’s
syndrome is characterized by miosis, partial
ptosis, apparent enophthalmos and anhidrosis.
Less constant features include facial flushing,
art erio lar or venular dilatatio n, tr ansient
lowering of intraocular pressure, hemi-atrophy
of the face and iris heterochromia (in congenital
Horner’s syndrome).2
Johann Friedrich Horner (1831-1886), a Swiss
ophthalmologist has been credited with the
description of this eponymous syndrome.3,4 He
de s c r ibed pto sis, miosis, apparent
enophthalmos, flushing, warmth and anhidrosis
on right side of the face in a 40-year-old woman.
By instilling belladonna (aropine) and calabar
(physostigmine) drops, he demonst r ated
paralysis of the dialator pupillae, along with
the paresis of the levator palpebrae superioris
and vasomotor paralysis and suggested that the
condition resulted from interruption of the
cervical sympathetic pathway.3,4 Edward
Selleck Hare (1812-1838) described a patient
with a tumour in left inferior triangular space
of the neck with miosis and ptosis. However,
he could not relat e t he se s igns to t he
inter r u p t ion of the symp at hetic nervo us
system.3 Claude Bernard (1830-1878) observed
that cutting the rabbit’s cervical sympathetic
nerve resulted in constriction of the pupil,
flushing and rise in the temperature of the ear
on that side. Based on these observations he
proposed that sympathetic nerves control the
Figure 1(C): Non-contrast computed tomography of the
chest (mediastinal window) showing a lobulated soft
tissue density lesion in the apex of the right lung
(asterisk); destruction of the first rib is also evident
(arrow head)
Figure 1(D): Photomicrograph of CT-guided tru-cut
biopsy specimen showing pleomorphic cuboidal to
columnar tumour cells arranged in ill-defined glandular
pa tter n (ar r ows) suggestive of aden oca r cinoma
(Haematoxylin and eosin, × 400)
Table 1: Common causes of Horner’s syndrome
Site of the lesion Common causes
Central Stroke
Tumours
Trauma
Demyelination
Pre-ganglionic Apical lung tumours (e.g., Pancoast tumour)
Subclavian artery aneurysm
Mediastinal tumours
Cervical rib
Iatrogenic (jugular cannulation, chest tube placement)
Post-ganglionic Internal carotid artery trauma, dissection, arteritis, aneurysm, thrombosis
Cavernous sinus thrombosis
Tumours
Source: reference 5
Horner’s syndrome due to Pancoast tumour Hari Krishna et al
152
blood circulation.4 The common causes of
Horner ’s syndrome are listed in Table 1.5
Pancoast tumour (also called superior sulcus
tumour) named after Henry Khunrath Pancoast,
a Radiologist from the United States of America
(USA), is a frequently encountered cause of
Horner’s syndrome.6 Identification of Horner’s
syndrome on physical examination is crucial
as it may sometimes be the only clue to a serious
underlying disease.
REFERENCES
1. Amonoo-Kuofi HS. Horner ’s syndrome revisited:
with an update of the central pathway. Clin Anat
1999;12:345-61.
2. Kong YX, Wright G, Pesudovs K, O’Day J, Wainer
Z, Weisinger HS. Horner syn drome. Clin Exp
Optom 2007;90:336-44.
3. Pearce JM. A note on Claude Bernard-Horner’s
syn dr ome. J Neur ol Ne ur os urg Psych i a tr y
1995;59:188-91.
4. Ross IB. The role of Claude Bernard an d others
in the discovery of Horner’s syndrome. J Am Coll
Surg 2004;199:976-80.
5. Walton KA, Buono LM. Horner syndrome. Curr
Opin Ophthalmol 2003;14:357-63.
6. Pancoast HK. Importance of careful roentgen-ray
investigations of apical chest tumors. JAMA
1924;83:1407-11.
Horner’s syndrome due to Pancoast tumour Hari Krishna et al
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Horner syndrome is an uncommon but important clinical entity, representing interruption of the sympathetic pathway to the eye and face. Horner syndrome is almost always diagnosed clinically, though pharmacological testing can be used to confirm the diagnosis. Imaging modalities such as PET, CT and MRI are important components of work-up for patients presenting with acquired Horner syndrome. Our patient’s presentation with Horner syndrome unmasked the causative superior sulcus squamous cell carcinoma and a coincidental lower lobe adenocarcinoma. Successful radical treatment of these cancers resulted in complete resolution of the syndrome and disease-free survival at 18 months. We review the anatomy and pathophysiology underlying this and other causes of Horner syndrome.
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Horner syndrome refers to the constellation of signs resulting from the interruption of sympathetic innervation to the eye and ocular adnexae. Classically, the clinical findings include a triad of ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis. The history, additional clinical examination features, and pharmacologic testing may help localize the lesion and suggest an etiology. An appropriate evaluation of Horner syndrome and a timely elucidation of the etiology may allow for a potentially life-saving intervention.
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There is an unusual but apparently infrequent type of intrathoracic growth occurring in the apical region, yet found with sufficient frequency in my experience to warrant a collective report of the cases encountered. The neoplastic condition is unusual for the reason that it produces referred nerve phenomena in the upper extremity which may be very misleading to the clinician and roentgenologist in their search for the cause; and when to these manifestations are added certain cervical sympathetic phenomena, the symptomatology of spinal cord tumor is closely simulated, especially in the absence of any apparent extraspinal etiologic factor. I have been fortunate enough to learn the exact nature of these growths from careful pathologic studies in two cases, and in all four cases there has been a most satisfactory correlation of clinical and roentgenologic data.In three of the four cases, an early diagnosis of the condition present was missed because
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A brief summary is presented of the life of Johann Friedrich Horner, the eminent Swiss ophthalmologist, renowned for describing the effects of paralysis of the human cervical sympathetic nerves. His early education, the quality of his professional training, and the influence of his mentors, notably Carl Ludwig and Albrecht von Graefe, contributed to his discovery of the syndrome. The full text of Horner's original work (translated by J. F. Fulton, 1929a, Arch. Surg. 18:2025-2039) is cited. The history of clinical and experimental work carried out on the autonomic nervous system prior to Horner's discovery is reviewed, including the studies of Pourfour du Petit (cited in Fulton, 1929a and Singer and Underwood, 1962, Clarendon); Hare, 1838, Lond. Med. Gaz. 23:16-18; Bernard (cited by Singer and Underwood); Budge (1853, Acad. de Sci., p.377-378); Mitchell et al. (1864, Lippincott). Hare and Mitchell et al. came close to making the discovery but were apparently hindered by their inability to interpret the signs they elicited in their patients. The experiments of Claude Bernard gave succinct accounts of the effects of damage to the cervical sympathetic nerves in animals, although there appears to be no evidence that he made similar observations in humans. Horner was the first to give a detailed, scientifically supported account and accurately interpret the signs of cervical sympathetic nerve damage in a human subject. The anatomy of the pathway is reviewed and the detailed structure of its central part updated. Evidence from computerized tomography (CT), magnetic resonance imaging (MRI), positron emission tomography (PET), and single-photon-emission computerized tomography (SPECT) studies have confirmed that reciprocally connected centers in the insular cortex, central nucleus of amygdala, hypothalamus, mesencephalic and pontine tegmentum, nucleus of tractus solitarius, and the ventrolateral medulla form the central pathway. The nucleus of tractus solitarius is probably the main reflex center for the sympathetic system, whereas the ventrolateral medulla serves as the pathway through which the central neurons influence the preganglionic neurons of the thoracolumbar outflow. Emotional and sensory inputs from the frontal and somatosensory cortices provide the inputs needed by the insula to drive the sympathetic nervous system to produce appropriate responses.