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Clinical features Patients with thyrotoxicosis may experience behavioral and personality
changes, such as psychosis, agitation, and depression. Less overt manifestations that are more
common in less severe thyrotoxicosis include anxiety, restlessness, irritability, and emotional
lability [10]. Insomnia is also common. Elderly patients may have a less activated presentation
with depression and lethargy, so-called apathetic thyrotoxicosis [1]. These behavioral
manifestations are accompanied by cognitive impairments, particularly impaired concentration,
confusion, poor orientation and immediate recall, amnesia, and constructional difficulties.
Seizures may accompany the encephalopathy of acute thyrotoxicosis and occasionally are the
presenting clinical feature [11]. They may be focal or generalized [11-14]. Tremor and
hyperreflexia with other pyramidal tract signs are also common features of the neurologic
examination in thyrotoxicosis [15]. (See 'Tremor' below and 'Motor neuron disease' below.)
The presentation of cognitive dysfunction in hyperthyroidism is usually subacute; however, a
more protracted course similar to a degenerative dementia has also been described [16]. In severe
thyrotoxicosis, a condition frequently referred to as thyroid storm, the neurologic presentation is
more fulminant, progressing if untreated through an agitated delirium to somnolence and
ultimately to coma [17]. In many of these cases there is an underlying stressor, such as sepsis,
trauma, or a recent surgical procedure. Seizures are more prominent in this setting and may
include status epilepticus [12,13,18]. Other clinical features of thyroid storm, such as
tachycardia, fever, and gastrointestinal symptoms, are commonly present (table 2).
Laboratory features There are no reports of abnormalities on magnetic resonance imaging
(MRI) or computed tomography (CT) neuroimaging studies. However, in one patient, single
photon emission CT (SPECT) demonstrated diffusely reduced cerebral uptake with an
accentuation in the temporoparietal regions bilaterally, which improved following resolution of
the hyperthyroid state [16].
Nonspecific electroencephalography (EEG) abnormalities have been reported in 43 percent of
patients with hyperthyroid encephalopathy [19]. EEG may demonstrate diffuse slowing,
bitemporal sharp waves, polyspike and slow wave discharges, or may be normal [11,14]. In
addition, an unusually high voltage with prolonged photic response and triphasic waves have
been described in individual patients [11,20].
Pathogenesis The mechanism of cognitive and behavioral dysfunction in hyperthyroidism is
not known. Improvement of some clinical features (attention and concentration) with betablocker therapy suggests a role for a hyperthyroid-induced hyperactive adrenergic system,
possibly disrupting the adrenergic pathways between the locus ceruleus and frontal lobe that
subserve attention and vigilance [16]. Others propose that hyperthyroidism may produce
oxidative stress, producing neuronal injury and hastening a presentation of degenerative or
vascular dementia [8].
The etiology of seizures in thyrotoxicosis is also not known. Animal studies have demonstrated
that exogenous administration of thyroxine lowers the seizure threshold. Elevated thyroxine
levels have also been associated with precipitating seizures in two patients with previously wellcontrolled juvenile myoclonic epilepsy [21].