A 50-year-old man presented with sudden onset voice changes, nasal regurgitation, nausea, and vomiting one day after suffering a severe head injury from a motor vehicle accident. Imaging showed resolving brain contusions and absence of blood flow in the left transverse and sigmoid sinuses, suggesting sinus thrombosis. Examination revealed palsies of the ninth, tenth, and eleventh cranial nerves on the left side. Head trauma can cause sinus thrombosis by direct compression or endothelial damage, leading to clot formation. The patient's symptoms resolved over one month with conservative management. Traumatic dural venous sinus thrombosis is a known complication of head injuries involving skull fractures near sinuses.

1. LATE ONSET JUGULAR FORAMEN
SYNDROME FOLLOWING HEAD TRAUMA
DR VINEET SAGGAR
CONSULTANT DEPARTMENT OF NEUROSURGERY
IVY HOSPITAL MOHALI

2. HISTORY
 A 50 year old man presented in our OPD
with sudden onset change of voice , nasal
regurgitation of fluids, nausea and vomiting
for past one day
 Patient had suffered severe head injury few
days back following RTA for which he was
admitted in a hospital where he remained in
unconsious state for few days and he was
discharged in fully consious state after 10 days
of admission in that hospital

3.  CT scans of previous admission showed
bifrontal contusions with surrounding edema
which were managed conservatively
 A week after his discharge patient suddenly
developed these problems.
 There was no history of fever , ear discharge
or any previous history of coagulation
abnormalities

4. CLINICAL EXAMINATION
 GPE of the patient was un remarkable
 Gcs was 15/15
 Examination of the cranial nerves revealed
- Absent gag reflex on the left side
- Lt pharyngeal arch was lower compared to rt.
side
- Deviation of uvula on rt side
- Indirect laryngoscopy revealed vocal cord palsy
on left side
- Shoulder shrugging was weak on left side

5.  All these features suggested involving of
9th, 10th and 11th cranial nerves on left side.
 Rest of the neurological examination was
normal

6. RADIOLOGICAL INVESTIGATIOS
- MRI Brain revealed resolving bifrontal
contusions with absence of flow void in left
transverse and sigmoid sinuses on t 2
weighted images suggestive of sinus
thrombosis
- C T angio was normal in arterial phase but
also revealed also revealed absence of flow in
in sigmoid and transverse sinuses
- C T also revealed a fracture at the base of
skull crossing jugular formamen on left side

7. Axial T2 flair image showing
hyperintense thrombus in
left sigmoid sinus

8. GRE IMAGES SHOWING THROMBUS
IN LEFT SIGMOID SINUS

9. T2 Axial images showing
hyperintensity in lt sigmoid
sinus

10. CT angiogram in late venous phase showing
absence of dye in left sigmoid sinus and fracture
across occipital bone reaching jugular foramen

11. Volume CT showing absence of
flow in sigmoid sinus

13.  Patient was managed conservatively
 There was no progression of symptoms over
next few days
 At one month follow up patient patients
symptoms had resolved .
 Hoarseness of voice had improved and he is
able to swallow liquids normally

14. ANATOMY OF JUGULAR FORAMEN
 It can be regarded as a hiatus between the
temporal and the occipital bones
 The foramen is situated so that its long axis is
directed from posterolateral to anteromedial
direction.

15. The jugular foramen is divided into three
compartments:
 Two venous and a neural or intrajugular
compartment.
 The venous compartments consist of a larger
posterolateral venous channel, the sigmoid
part, which receives the flow of the sigmoid
sinus, and a smaller anteromedial venous
channel,the petrosal part, which receives the
drainage of the inferiorpetrosal sinus

17. The structures that traverse the jugular foramen are
- The sigmoid sinus and jugular bulb,
- The inferior petrosal sinus
- Meningeal branches of the ascending pharyngeal
and occipital arteries,
- The glossopharyngeal, vagus, and accessory nerves
with their ganglia, the tympanic branch of the
glossopharyngeal nerve (Jacobson’s nerve), the
auricular branch of the vagus nerve (Arnold’s nerve),
- The cochlear aqueduct.

18. Mechanism of thrombosis
 Following head injury, skull fractures or
intracranial hematomas can cause thrombosis
either by direct compression of the sinus
OR
 Endothelial damage within the sinus can cause
the activation of the coagulation system
resulting in sinus occlusion.
 Uncommonly, sinus thrombosis can occur after
mild closed head injury with sutural diastasis

19. Mechanism of cranial nerve
palsies
 In the early literature, several cranial nerve
syndromes in CVT have been identified and
attributed to extension of thrombosis into
contiguous venous tributaries, presumably
leading to direct pressure palsy of the nerves
lying in proximity to the clot.
 Recently that Kuehnen et al have suggested
that local stasis in the cranial nerve veins
draining into the transverse sinus might cause
temporary nerve dysfunction.

20. DISCUSSION
The common causes of intracranial dural
venous sinus thrombosis include
 head and neck infections,
 pregnancy and
 puerperium, use of oral contraceptives,
 dehydration
 Rarely trauma

21.  Although there are numerous case reports
only a few case series of patients with dural
venous sinus thrombosis (DVST) after blunt
head trauma have been reported in the
literature
 Thus, the frequency and associated morbidity
of DVST in patients with acute blunt head
trauma are not well understood

22.  Approximately 206 cases of traumatic DVST
have been reported in the literature
 For 131 of these cases, information regarding
associated skull fractures has been provided
 Skull fractures are present in 105 (80.2%) of
the cases. In the remaining 26 cases, a
diagnosis of DVST was rendered an average
of 9 days (range, 1–42 days) after the trauma.

23.  Most of these have been isolated case reports or case
series mainly pretainnig to pediatric age group
 Commonly, increased intracranial pressure signs such
as nausea, vomiting and headache are present. The
compensatory function of the venous collateral
system is the main factor that determines the DST
diagnosis and also affects prognosis.
 When compared to adults, incomplete growth of
venous collaterals in children explain higher
frequency of these cases being symptomatic and
reported in children

24.  Largest study in adults to date is:
“ Prevalence of Traumatic Dural Venous Sinus
Thrombosis in High-Risk Acute Blunt HeadTrauma
Patients Evaluated with Multidetector CT
Venography”
by DelgadoAlmandoz et al Radiology: Volume 255:
Number 2—May 2010

25. INCLUSION CRITERIA
 Patients with acute blunt head trauma are
examined with multidetector CT venography for
possible traumatic DVST if there was
(a) a skull fracture near a dural venous sinus or
jugularbulb or
(b) a high index of clinical suspicion such as that in
patients with persistent headache, vomiting,
papilledema, seizures, or other signs of increased
intracranial pressure.
In patients who are also deemed to be at risk for
arterial injury, multidetector CT venography is
performed as a delayed acquisition of the head
after multidetector CT angiography of the cervical
vasculature.

26. OBSERVATIONS
 Traumatic occlusive DVST was found in 31
(19.5%) of the 159 patients with skull
fractures .
 The patients with skull fractures that
extended to at least one dural venous sinus or
jugular bulb had an overall risk of traumatic
DVST of 40.7%

27.  The risk of injury to the transverse
sinuses, sigmoid sinuses, and jugular bulbs to
be higher with fractures of the petrous
temporal bone,
 The risk of injury to the superior sagittal
sinus to be higher with fractures of the
occipital bone

28.  Patients with traumatic occlusive DVST who
experience neurologic deterioration, performing
either MR imaging or follow-up nonenhanced CT
may be useful in assessing for an associated
hemorrhagic venous infarction
 A small minority of patients with occlusive DVST
were treated with anticoagulation. This is
probably because of the high frequency of
concurrent intracranial hemorrhage in this
patient population and illustrates the inherent
difficulty in managing their treatment

29. CONCLUSIONS
 Traumatic DVST is a common finding
complicating head injuries with fractures
extending across venous sinuses
 Multidetector CT angiography in venous phase is
most useful in establishing the diagnosis
 Treatment in most of the cases with mild
neurological deficits is conservative
 Treatment in patients with raised ICP may
involve anticoagulation or thrombolysis but their
respective roles require further studies to be fully
established.

30. THANK YOU