PAROXYSMAL SYMPHATHETIC

HYPEREACTIVITY
 Epidemiology
• 80% due to traumatic brain injury
• PSH is especially associated with diffuse axonal injury
• 10% due to anoxic brain injury
• 5% due to stroke ( especially large intracranial or subarachnoid haemorrhage)
• 5% dye to othe pathologies
• Acute hydrocephalus Risk factors
• Tumors • Severity of initial injury
• Hypoglycemic brain injury • Younger age
• Infection ( encephalitis) • Male sex
• Cerebral fat embolim syndrome
• Autoimmune encephalitis
PATHOPHYSIOLOGY
Excitatory:Inhibitory
Ratio (EIR) model
Disconnection of descending
inhibition

Spinal circuit excitation

Non-noxious stimuli perceive

as noxious stimuli

increased and prolonged

response
CLINICAL • The primary clinical feature of PSH is
FEATURES simultaneous, paroxysmal transient
increases in sympathetic, as well as
6 CORE FEATURES motor activity
Tachycardia • PSH is a complex syndrome with
Tachypnea, individual spectrum of clinical
Hypertension, symptoms
Hyperthermia, • Hypertension, diaphoresis, and
dystonia, can be considered as
Hyperhidrosis, predictive signs of pediatric PSH,
Posturing relative to adults
 • Onset varied, average cases onset in 1 week post injury
Onset • The first stage is often asymptomatic due to the heavy sedation

• .[ • Episodes vary in duration and occurrence. Episodes can last as

little as a few minutes or as long as ten hours, and they can
Duration occur multiple times a day.
• Episode duration has been seen to average 30.8 minutes and
occur five to six times a day.
• Episodes can occur naturally or arise from external triggers.
Trigger • Common triggers include pain or stimulation ,suctioning, body
factors turning or movements, and bladder distention.

• Symptoms of PSH can last from weeks to years following initial

onset.
Recurrence • As episodes persist over time, they have been found to become
less frequent in occurrence but last for prolonged periods
 Identify
PSH
• Currently, the Paroxysmal
Sympathetic Hyperactivity-
Assessment Measure (PSH-AM)
scale consists of two separate
constructs:
(1) The clinical feature scale (CFS),
to identify the intensity of
cardinal features, Paediatric
PSH scoring reference)
(2) the diagnosis likelihood tool
(DLT), to evaluate the
likelihood of the presence of
PSH
 Role of imaging in PSH
Magnetic resonance imaging (MRI)
Suggests that PSH is more likely to be found
in patients with deep structural as well as
diffuse brain damage, while grouping lesions
into three different classifications (cortical
and subcortical white matter, corpus
callosum or diencephalon, and dorsolateral
aspect of the midbrain and upper pons
• Because the pathology of PSH is unclear,
these findings are unable to precisely
identify the neuroanatomical
characterization bias of PSH and thus
cannot provide a confirmed diagnosis.
 Treatment
• Traditional views hold that obstacles to the development of PSH
treatment are the following
• (1) insufficient understanding of brain regions,
• (2) no definite relationship between neurotransmitters or hormones and
clinical symptoms
• (3) lack of standardized measures to assess the curative effect
• (4) insufficient evidence from clinical trials regarding the benefits of
intervention for long-term outcomes
• Treatment divided into 2 category
• Pharmacological
• Non pharmacological
 Pharmacological treatment
• Medication may be given intravenous and rapid onset ( ideally
symptom
within minutes )
elimination
• PSH symptoms such as hyperthermia and hypertension can
cause 2ry brain injury in not resolve
•used for decreasing the frequency and intensity of PSH patients’
symptom symptoms
prevention •Often given as oral medication with can continue in long term
basis

it must begin with the recognition that certain symptoms are

refractory
insensitive to treatment and some symptoms (e.g., hyperthermia
treatment
or hypertension) can lead to secondary injury
 Non pharmacological treatment

• Avoid external stimuli

• Adequate hydration and nutrition
• Pain management
• Maintain normal temperature
 Reference
• Zheng R-Z, Lei Z-Q, Yang R-Z,Huang G-H and Zhang G-M (2020) Identification
and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic
Brain Injury. Front. Neurol. 11:81. doi: 10.3389/fneur.2020.00081
• The Impact of Paroxysmal sympathetic Hypereactivity following traumatic
brain injury on ICU By Kimberly S. Meyer B.S.N., University of Louisville, 1992
M.S.N., University of Kentucky, 2002
• Paroxysmal Sympathetic Hyperactivity: the storm after acute brain injury,
Geert Meyfroidt zz Department of Intensive Care MedicineUniversity
Hospitals Leuven, MD, Ian J Baguley Westmead HospitalBrain Injury
Rehabilitation Service, MBBS, DavidKMenon,FMedSci Division of
AnaesthesiaUniversity of Cambridge